Ambulatory blood pressure monitoring in renal transplantation: should ABPM be routinely performed in renal transplant patients?

In renal transplant recipients, hypertension is common and associated with increased cardiovascular and allograft rejection risks. Ambulatory blood pressure monitoring is required for its accurate diagnosis and adequate treatment, as it clearly offers several advantages over office or casual blood pressure measurements. First, it correlates better with target-organ damage and with cardiovascular mortality. Second, ambulatory blood pressure monitoring can eliminate "white coat" hypertension. Most important is the identification of nocturnal hypertension, an independent cardiovascular risk factor. A circadian nondipping pattern is often found in renal transplant recipients, most probably resulting from cyclosporine A and persistent fluid overload in the early posttransplant phase (approximately 70% prevalence), but reflecting an underlying renal (parenchymal or vascular) allograft disease when persistent (approximately 25% prevalence) beyond the first year posttransplant.     

Ambulatory blood pressure monitoring in renal transplant patients: should it be routinely performed?

Introduction

Arterial hypertension is common among kidney transplant patients. It increases cardiovascular risk and is a factor for progression of renal failure. Our objective was to perform ambulatory blood pressure monitoring (ABPM) in renal transplant patients with office hypertension.

Methods

Patients were divided into 2 groups according to their mean ABPM blood pressures with treatment: well-controlled hypertension (blood pressure [BP] <130/85 mmHg), and poorly controlled hypertension (BP > 130/85 mmHg). A “nondipper pattern” was defined as a decrease of <10% or an increase, and a “raiser pattern,” in which mean blood pressure was greater during the nocturnal than the diurnal period. “White coat effect” was considered when the mean of 3 BP measurements in the clinic was >140/90 mmHg among well-controlled hypertensive patients as documented by ABPM.

Results

ABPM was performed in 53 patients: 25 (47%) “well-controlled hypertensives” and 28 (53%) “poorly controlled hypertensives.” Of the latter, 24 (85%) showed a nondipper or raiser pattern with only 4 revealing dipper patterns. We compared well-controlled with poorly controlled hypertensives. The latter cohort were older (54.4 ± 9.3 vs 45.5 ± 13.8 years; P = .009), received grafts from older donors (56.7 ± 15.0 vs 45.8 ± 17 years; P = .02); had worse renal function measured by serum creatinine (1.7 ± 0.5 vs 1.4 ± 0.4 mg/dL, P = .03) or the Modification of Diet in Renal Disease (MDRD) = 4 formula (41.8 ± 14.0 vs 55.4 ± 20.5 mL/min/1.73 m²; P = .009), and displayed more proteinuria (0.30 ± 0.33 vs 0.18 ± 0.10 g/d, P = .08). Nondipper or raiser patients showed a higher mean body mass index (27.1 vs 21.7 kg/m²; P = .04). Among 25 well-controlled patients, 11 presented “white coat phenomenon.”

Conclusion

We observed an important “white coat” effect, a large prevalence of uncontrolled nocturnal hypertension, and a small but important incident of “masked hypertension.” Factors related to hypertension control were patient age, donor age, renal function, induction use, and proteinuria.     

Dyslipidemia in children with CKD: should we treat with statins?

Dyslipidemia has been shown to be a risk factor for increased cardiovascular morbidity and mortality in adult patients with chronic kidney disease (CKD) stages 2–4. In patients on dialysis, a paradoxical correlation has been found between low cholesterol values and increased mortality rates. No data exist in children. Treatment with statins has been convincingly shown to both reduce blood lipid levels and mortality rates from cardiovascular disease in adult patients in CKD stages 2–4. There is no strong literature support for treating patients on dialysis or after having had a transplant. Data on benefits of statin therapy do not exist in children with CKD. There are many differences between adult and paediatric kidney patients, and I caution on extrapolating the findings in adult patients to children. Studies are thus needed to evaluate the benefits and potential problems of statin treatment in children with CKD.     

Does JC polyomavirus cause nephropathy in renal transplant patients?

Introduction

BK polyomavirus (BKV) reactivation characterized by active viruria occurs in 23%-57% of renal allograft recipients and BKV-associated nephropathy in as many as 8% of renal allograft recipients. Only a few cases of nephritis have been attributed to JC polyomavirus (JCV) with limited information about JCV replication and its impact on graft function and survival of kidney transplant patients. We sought to determine the prevalence of BKV and JCV replication, the risk factors associated with viral reactivation, and their implications for the development of polyomavirus nephropathy (PVN) among renal transplant patients.

Materials and Methods

The study included 186 kidney transplant recipients who were transplanted between 2005 and 2009 with a 1-year follow-up. If the urine polymerase chain reaction (PCR) was positive, we performed a PCR on blood. If this was positive or renal dysfunction was present, we performed a renal biopsy.

Results

Viruria was positive in 72 cases (39%) and viremia in 12 (6.5%); including, 3 patients (1.6%) who developed PVN. In the patients with viruria, BKV was detected in 47% and JCV in 46%; both were detected in 7%, although the combination of viremia and nephropathy were caused by BKV in all cases.

Conclusion

In renal transplant patients, the incidence of BKV and JCV viruria was similar, although in our series the JCV serotype did not cause viremia or PVN. Our experience suggested that JCV did not have the ability to cause PVN.     

Why should we implement living donation in renal transplantation?

BACKGROUND: Renal transplantation started with living donor transplants. However, after the introduction of cyclosporine, the improved results of kidney transplants from cadaveric donors have raised controversy regarding the use of living donors. There are various reasons as to why some transplant centers tend to refuse living donation: first of all, the possibility that unilateral nephrectomy can be harmful to a healthy individual. SUBJECTS AND METHODS: By reviewing the medical literature on the various aspects of living donation, postoperative mortality in connection with living donation has been calculated to be 1:3,000. RESULTS: Long-term follow-up investigations of donors demonstrated that the risk of progressive renal failure, hypertension, and proteinuria was not increased by nephrectomy per se, but other causes were responsible for that in occasional patients. From these studies, one can conclude that unilateral nephrectomy is not harmful to a healthy individual. In addition, there are other valid reasons to expand living donation: 1) the need for cadaveric donor kidneys for transplantation far exceeding the supply; 2) the better kidney quality from living donors due to the shorter ischemia time, the lack ofagonal phase and cytokines release that follows brain death; 3) the continuing improved results of kidney transplants from living donors in comparison with those from cadaveric donors in the cyclosporine era also. This appears to be true also for kidney transplants from unrelated living donors in spite of complete incompatibility with recipients. 4) Pre-emptive transplantation, based on living donors, not only avoids the risks, cost, and inconvenience of dialysis, but is also associated with better graft survival than transplantation after a period of dialysis, particularly within the live donor cohort. CONCLUSIONS: In conclusion, living donor transplants should be part of any transplant center's activity. To encourage living donation, every center should have a formal recipient family education program in conjunction with national organ donation campaigns.     

Interstitial cystitis: how should we diagnose it and treat it in 2004?

PURPOSE OF REVIEW: During the last 2 years, two international and two European meetings have taken place and a European Society formed dealing only with interstitial cystitis. A separate committee for interstitial cystitis was formed during the last WHO International Consensus Meeting on urinary incontinence. As a consequence, new concepts and recommendations are evolving, for example the nomenclature is changing from interstitial cystitis to painful bladder syndrome/interstitial cystitis. RECENT FINDINGS: At an international meeting in Kyoto, the scientific basis for diagnosis and treatment of painful bladder syndrome/interstitial cystitis was reviewed, confirming the poor evidence for many diagnostic procedures and treatments. There are two main reasons for this: an internationally accepted definition is lacking and the disease is rare, making clinical trials difficult. A meeting in Copenhagen resulted in a standardization of the procedures for evaluation and the creation of a European Society for the Study of Interstitial Cystitis. Increased concentration of nitric oxide in the urine of patients with Hunner's ulcer may help to separate ulcer from non-ulcer patients. A prospective, randomized, placebo-controlled multicenter study failed to show a statistically significant effect of the antihistamine hydroxine or pentosan polysulfate sodium compared with placebo. The study confirmed the difficulties in recruiting patients for large-scale trials, which could be one of the reasons for the negative result. The effect of the traditional treatment with amitriptyline was confirmed in a prospective, placebo-controlled study. SUMMARY: Standardized evaluation of patients with painful bladder syndrome/interstitial cystitis will benefit both patients and science. An internationally accepted definition of the condition appears to be in sight, which will make epidemiological and research studies easier.     

Acute renal failure - how and when to treat?

Acute renal failure is a common condition in intensive care units. The negative impact of acute renal failure on mortality has been demonstrated in recent studies. All critically ill patients should be regarded as a high risk population for renal failure. The optimization of intravasal fluid status and mean arterial pressure are preventive strategies in these patients. The use of nephrotoxic drugs (including radiocontrast media) should be avoided if possible. In cases of established acute renal failure today therapeutic strategies are still limited to best supportive care. The use of diuretics can facilitate fluid balance, however they seem to have an adverse effect on excretional renal function. A number of patients with acute renal failure need extracorporal renal support. Overload of potassium or fluids, severe acidosis, uremic pericarditis or uremic encephalopathy are urgent indications for the start of renal replacement therapy. Small randomized trials give some evidence that an early start of renal replacement therapy may be beneficial in critically ill patients. In this patient group renal replacement therapy should be considered when serum urea concentrations exceed 100mg/dl and/or when early signs of indications mentioned above are present. Large randomized multicenter trials have shown that a favourable effect on mortality can only be achieved when renal replacement therapy is supplied with a sufficient dose. Daily hemodialysis or continuous hemofiltration with a filtrate volume of 35ml/kg/h is regarded as a standard of care. There is still controversy whether continuous hemofiltration is superior to intermittent hemodialysis. Large meta-analyses could not show a difference in mortality with either one of the two therapy options.     

Does subclinical rejection contribute to chronic rejection in renal transplant patients?

Renal allograft biopsies have traditionally been performed in the setting of acute graft dysfunction. However, several groups have performed graft biopsies at times of stable graft function, and more recently, after treatment of rejection episodes. Surprisingly, unequivocal histologic criteria for acute rejection have been demonstrated in a high proportion of these protocol biopsies. The Winnipeg Transplant Group has documented the high prevalence of clinically silent inflammatory infiltrates in early protocol biopsies, and demonstrated their inflammatory and cytotoxic potential by immunohistochemical and molecular biological techniques. Furthermore, in a randomized trial, our group has demonstrated that subclinical rejection, if untreated, is associated with the development of early chronic pathology and late graft dysfunction. In this overview, we will summarize the early data on subclinical allograft inflammation, present the experience of the Winnipeg Transplant Group, and discuss the possible implications of subclinical rejection on the development of chronic rejection.     

Fulminating varicella despite prophylactic immune globulin and intravenous acyclovir in a renal transplant recipient: should renal patients be vaccinated against VZV before transplantation?

We describe a case of fulminating varicella despite prophylactic immune globulin and intravenous acyclovir in a renal transplant recipient. This promoted a survey of all 383 adult patients awaiting a renal transplant in Scotland, which showed a low level of Varicella zoster virus (VZV) awareness but a willingness to consider vaccination if non immune. 359/363 serum samples tested were seropositive for VZV antibody giving a susceptibility to VZV of 1.2%. Although data on vaccination in adults with chronic kidney disease are limited, expert opinion is of the view that the benefits of vaccinating immunocompetent seronegative patients before transplantation are likely to outweigh the risks. We believe that adult patients awaiting a transplant in the UK should be tested for their susceptibility to VZV and that early vaccination should be offered to those who are both immunocompetent and seronegative.