Renal artery stenosis stenting with unmasking and embolisation of a renal arteriovenous fistula.

A man in his 70s was presented to the emergency department with uncontrollable hypertension and worsening renal function on a background of atherosclerosis-related bilateral renal artery stenosis. Following progressive deterioration in renal function and refractory hypertension, the patient was referred to interventional radiology for consideration of renal artery stenting. Following stenting of the right renal artery, a large renal arteriovenous fistula became apparent, which required emergent embolisation. Both procedures were successful, with excellent clinical and radiological responses.

Left ventricular torsion changes post kidney transplantation.

BACKGROUND: To quantify changes of left ventricular (LV) torsion in patients' pre and post kidney transplantation. METHODS: A prospective study was conducted on 48 patients who received kidney transplantation for end stage renal disease and without myocardial infarction. The rotation, twist and torsion of LV were studied pre and post kidney transplantation (6 months post transplantation) using velocity vector imaging by echocardiography. The data is expressed as mean ± standard deviation and compared by paired t-test at the p < 0.05 significance level. RESULTS: Six months post kidney transplantation, left ventricular ejection fraction (from 40.33 ± 11.42 to 61.00 ± 13.68%), ratio of mitral early and late diastolic filling velocity (from 1.04 ± 0.57 to 1.21 ± 0.52), rotation of basal LV (from 4.48 ± 2.66 to 5.65 ± 2.64 degree), rotation of apical LV (from 4.27 ± 3.08 to 5.50 ± 4.25 degree), LV twist (8.75 ± 4.45 to 11.14 ± 5.25 degree) and torsion (from 1.06 ± 0.54 to 1.33 ± 0.61 degree/cm) were increased significantly (p < 0.05). Interventricular septum thickness (from 11.67 ± 2.39 to 9.67 ± 0.48 mm), left ventricular mass index (from 104.00 ± 16.47 to 95.50 ± 21.44 g/m(2)), systolic blood pressure (from 143.50 ± 34.99 to 121.50 ± 7.09 mmHg), serum blood urea nitrogen (from 42.40 ± 7.98 to 30.43 ± 13.85 mg/dL) and creatinine (from 4.53 ± 1.96 to 2.73 ± 2.57 mg/dL) were decreased significantly (p < 0.05). CONCLUSION: Kidney transplantation in end stage renal disease without myocardial infarction results in improvement in left ventricular structure, function and myocardial mechanics as detected by echocardiography and velocity vector imaging. Velocity vector imaging provided valuable information for detection and follow-up of cardiac abnormalities in patients with end stage renal disease.

Polyomavirus JC urinary shedding in kidney and liver transplant recipients associated with reduced creatinine clearance.

BACKGROUND: Polyomavirus reactivation can cause significant morbidity in solid organ transplant recipients, particularly BK virus (BKV) in kidney transplant patients. Less is known about dynamics of John Cunningham virus (JCV) in nonkidney organ transplant patients. METHODS: We examined the frequency of urinary shedding of polyomaviruses BKV and JCV and their relationship to creatinine clearance (CrCl) in a longitudinal study of 41 kidney and 33 liver transplant recipients. RESULTS: Any polyomavirus urinary shedding was more frequent in liver than kidney recipients (64% vs 39%; P= .03). JCV was excreted more frequently by liver than kidney recipients (71% vs 38%), whereas BKV was shed more often by kidney than liver patients (69% vs 52%). Mean JCV loads were significantly higher than those of BKV in both patient groups (P< .0001). Lower mean CrCl values were significantly associated with JCV shedding in both kidney and liver recipients (P< .001). CONCLUSIONS: These findings suggest that BKV and JCV display different patterns of reactivation and shedding in kidney and liver transplant patients and that JCV may have a role in renal dysfunction in some solid organ transplant recipients.

Relationship between inpatient hyperglycemia and insulin treatment after kidney transplantation and future new onset diabetes mellitus.

BACKGROUND AND OBJECTIVES: Approximately two-thirds of kidney transplant recipients with no previous history of diabetes experience inpatient hyperglycemia immediately after kidney transplant surgery; whether inpatient hyperglycemia predicts future new onset diabetes after transplant (NODAT) is not established. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: A retrospective study was conducted to determine the risk conferred by inpatient hyperglycemia on development of NODAT within 1 year posttransplant. All adult nondiabetic kidney transplant recipients between June 1999 and January 2008 were included. Posttransplant inpatient hyperglycemia was defined as any bedside capillary blood glucose > or = 200 mg/dl or insulin therapy during hospitalization. NODAT was defined as HbA1C > or = 6.5%, fasting venous serum glucose > or = 126 mg/dl, or prescribed diet or medical therapy for diabetes mellitus. RESULTS: The study cohort included 377 patients. NODAT developed in 1 (4%) of the 28 patients without inpatient hyperglycemia, 4 (18%) of the 22 patients with inpatient hyperglycemia but not treated with insulin, and in 98 (30%) of the 327 of the patients who were diagnosed with inpatient hyperglycemia and were treated with insulin. In adjusted analyses, requirement of insulin therapy during hospitalization posttransplant was associated with a 4-fold increase in NODAT (relative risk 4.01; confidence interval, 1.49 to 10.7; P = 0.006). CONCLUSION: Development of inpatient hyperglycemia after kidney transplantation in nondiabetic patients significantly increased the risk of NODAT. Additionally, we observed a significantly increased risk of cardiovascular events in patients who developed NODAT.

Altered Na(+) currents in atrial fibrillation effects of ranolazine on arrhythmias and contractility in human atrial myocardium.

OBJECTIVES: We investigated changes in Na(+) currents (I(Na)) in permanent (or chronic) atrial fibrillation (AF) and the effects of I(Na) inhibition using ranolazine (Ran) on arrhythmias and contractility in human atrial myocardium. BACKGROUND: Electrical remodeling during AF is typically associated with alterations in Ca(2+) and K(+) currents. It remains unclear whether I(Na) is also altered. METHODS: Right atrial appendages from patients with AF (n = 23) and in sinus rhythm (SR) (n = 79) were studied. RESULTS: Patch-clamp experiments in isolated atrial myocytes showed significantly reduced peak I(Na) density ( approximately 16%) in AF compared with SR, which was accompanied by a 26% lower expression of Nav1.5 (p < 0.05). In contrast, late I(Na) was significantly increased in myocytes from AF atria by approximately 26%. Ran (10 mumol/l) decreased late I(Na) by approximately 60% (p < 0.05) in myocytes from patients with AF but only by approximately 18% (p < 0.05) in myocytes from SR atria. Proarrhythmic activity was elicited in atrial trabeculae exposed to high [Ca(2+)](o) or isoprenaline, which was significantly reversed by Ran (by 83% and 100%, respectively). Increasing pacing rates from 0.5 to 3.0 Hz led to an increase in diastolic tension that could be significantly decreased by Ran in atria from SR and AF patients. CONCLUSIONS: Na(+) channels may contribute to arrhythmias and contractile remodeling in AF. Inhibition of I(Na) with Ran had antiarrhythmic effects and improved diastolic function. Thus, inhibition of late I(Na) may be a promising new treatment option for patients with atrial rhythm disturbances and diastolic dysfunction.

Successful transplantation of a split crossed fused ectopic kidney into a patient with end-stage renal disease.

Potential donors with congenital renal anomalies but normal renal function are often overlooked because of a possible increase in technical difficulty and complications associated with the surgery. However, as the waiting list for a deceased donor kidney transplant continues to grow, it is important to consider these kidneys for potential transplant. This paper describes the procurement of a crossed fused ectopic kidney, and subsequent parenchymal transection prior to transplantation as part of a combined simultaneous kidney pancreas transplant. The transplant was uncomplicated, and the graft had immediate function. The patient is now two years from transplant with excellent function.

Immunosuppression in simultaneous pancreas-kidney transplantation: progress to date.

Simultaneous pancreas-kidney transplantation (SPKT) is the treatment of choice for patients with end-stage renal failure due to type 1 diabetes mellitus. With advances in surgical techniques and immunosuppression management, outcomes have improved, with current 1- and 10-year pancreas graft survival rates of 86% and 53%, respectively. Induction therapy with either alemtuzumab or rabbit antithymocyte globulin (rATG) in combination with a calcineurin inhibitor (CNI) and mycophenolate mofetil (MMF) or sirolimus appears to be safe and effective in the setting of rapid steroid withdrawal (RSW), with excellent graft survival and low rejection rates. There are no large randomized trials between alemtuzumab and rATG to determine whether one is better than the other. Anti-interleukin (IL)-2 receptor antibody induction and no induction in combination with a CNI, MMF or sirolimus, and prednisone have demonstrated excellent graft survival rates but are associated with a higher incidence of acute rejection. The efficacy of anti-IL-2 receptor antibodies or no induction in the setting of RSW is unproven. Both of the CNIs, ciclosporin and tacrolimus, are effective in preventing acute rejection in SPKT recipients; however, pancreas allograft survival may be better with tacrolimus. MMF is more effective than azathioprine in preventing acute rejection. Sirolimus appears to be effective in preventing acute rejection, but the combination of sirolimus with a CNI may accentuate the nephrotoxicity of the CNI. RSW with induction therapy is safe and effective in SPKT recipients, but longer follow-up data on outcomes are needed. Recent analysis of registry data shows that most transplant centres are using an induction agent followed by a combination of tacrolimus, MMF and corticosteroids in SPKT recipients.

Increased prevalence of reduced estimated glomerular filtration rate in chronic hepatitis C patients.

BACKGROUND: To investigate the prevalence and severity of reduced estimated glomerular filtration rate (eGFR) in patients with chronic hepatitis C (CHC). METHODS: Medical record review of 831 consecutive CHC patients seen in our clinic between July 2000 and August 2003; eGFR was estimated using the abbreviated Modification of Diet in Renal Disease (aMDRD) equation. The stage of kidney disease was determined based on eGFR expressed in milliliters per minute per 1.73 m(2): stage 1 (signs of kidney damage but normal or elevated (eGFR >or= 90), stage 2 (eGFR 60-89), stage 3 (30-59), stage 4 (eGFR 15-29), stage 5 (eGFR < 15 or dialysis-dependent). RESULTS: A total of 522 patients had available data with using the aMDRD equation, 51% had abnormal eGFR (stage 1, 4.6%; stage 2, 36.4%; stage 3 or 4, 6.1%; stage 5, 3.8%). Of 190 patients with stage 2 kidney disease, 189 patients (99.5%) had normal serum creatinine and only one patient (0.5%) had elevated creatinine concentrations (>1.4 mg/dl). Of the 32 patients with stage 3 or 4 disease, 20 (62.5%) had a normal serum creatinine concentration. Of 349 patients without diseases known to cause renal insufficiency, 38% had stage 2-4 renal disease. In a subset of these patients, 95/522 (18%) the measured creatinine clearance showed good correlation with their aMDRD (R = 0.47, (p < 0.0001). CONCLUSIONS: In CHC patients, a normal serum creatinine concentration does not assure normal kidney function. Estimation of eGFR with the aMDRD equation is a more accurate method of identifying patients with chronic kidney disease and reduced eGFR. Therefore, CHC patients should be screened more rigorously for chronic kidney disease because of the high prevalence of reduced eGFR. Lastly, in all CHC patients, the aMDRD eGFR should be used in each encounter with these patients when assessing their renal function irrespective of their serum creatinine.

Hyperglycemia during the immediate period after kidney transplantation.

BACKGROUND AND OBJECTIVES: Hyperglycemia and new-onset diabetes occurs frequently after kidney transplantation. The stress of surgery and exposure to immunosuppression medications have metabolic effects and can cause or worsen preexisting hyperglycemia. To our knowledge, hyperglycemia in the immediate posttransplantation period has not been studied. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We conducted a retrospective, observational study to characterize the prevalence and assess the pharmacologic management of hyperglycemia in kidney transplant recipients who underwent transplantation at our center between June 1999 and December 2006. Data were abstracted from electronic and pharmacy databases. RESULTS: The study cohort included 424 patients (mean age 51 yr; 58% men; 25% with pretransplantation diabetes). All patients with and 87% without pretransplantation diabetes had evidence of hyperglycemia (bedside glucose >or=200 mg/dl or physician-instituted insulin therapy), whereas the prevalence of hypoglycemia was low (4.5%). Hyperglycemia was sustained throughout hospitalization. All patients with and 66% without pretransplantation diabetes required insulin at hospital discharge. Patients with pretransplantation diabetes were treated primarily with short-acting insulin during the first 24 h after transplantation but were transitioned to long-acting insulin as the hospital stay progressed. CONCLUSIONS: Investigators have historically attempted to identify hyperglycemia after hospital discharge. Our data indicate that a substantial number of patients without pretransplantation diabetes develop hyperglycemia and require insulin during the hospital phase of their care immediately after kidney transplantation. Prospective studies are needed to delineate factors that contribute to development of new-onset diabetes after transplantation among patients with transient hyperglycemia.

Plasmapheresis therapy for rare but potentially fatal reaction to rituximab.

Rituximab (Rituxan), a genetically engineered chimeric murine and human IgG1 monoclonal antibody directed against CD20 antigen, is an emerging drug used for a wide spectrum of disease processes and found to be relatively safe. We report a near-fatal reaction to rituximab, which started 30 min after infusion and worsened over 24 to 48 h, resulting in hemodynamic and respiratory compromise that necessitated both intubation and high-dose vasopressors. Subsequent treatment with plasmapheresis helped stabilize and improve the patient's clinical condition, and the patient was discharged home on hospital day 5. There is no specific treatment for these severe and sometimes fatal reactions except supportive care with plasmapheresis. With the increased use of rituximab therapy in the medical management of numerous diseases, those in the medical community need to be cognizant of the rare fatal or near-fatal infusion reaction and the benefit that may accrue from plasmapheresis therapy.

Clinical factors associated with graft fibrosis in kidney-transplant recipients on steroid-avoidance immunosuppression.

BACKGROUND: Recent studies have documented good patient and graft outcomes and a low risk of acute rejection with steroid-avoidance immunosuppression in kidney-transplant recipients, but the risk of progressive graft fibrosis is not well studied. METHODS: All adult primary kidney transplant or combined kidney and pancreas transplant recipients on steroid avoidance immunosuppression were eligible for study. All recipients received induction with antithymocyte globulin or basiliximab. Corticosteroids were stopped after day 4 post-transplantation. Patients were maintained with tacrolimus and mycophenolate mofetil. Protocol biopsies were done at reperfusion and at one, four, and 12 months after transplantation. RESULTS: Eighty one-yr protocol biopsies with adequate specimens were obtained from 132 kidney or kidney-pancreas transplant recipients. Fifteen (19%) of the biopsies showed moderate to severe graft interstitial fibrosis (GIF) (Banff ci score > or = 2). Recipients with GIF were older, had lower body mass index, greater human lymphocyte antigen (HLA) mismatch, older donors, serum creatinine > or = 1.6 mg/dL at one month, a Banff ci score > 0 on one-month biopsy, BK nephropathy, and interstitial cellular infiltrates on the one-yr biopsy. In the unadjusted logistic regression analysis, BK nephropathy, serum creatinine > or =1.6 mg/dL at one month, recipient age, Banff ci score > 0 on one-month biopsy, and donor age were the only variables associated with a higher risk of GIF on the one-year biopsy. In the multivariate logistic regression model adjusted for these variables, BK nephropathy, serum creatinine > or = 1.6 mg/dL at one month after transplantation, and recipient age were independently associated with the risk of GIF on the one-year biopsy. CONCLUSION: In this small study of primary kidney or combined kidney-pancreas transplant recipients on steroid-avoidance immunosuppression, we found that 19% had GIF on a one-year protocol biopsy. BK nephropathy, serum creatinine > or = 1.6 mg/dL one month after transplantation, and recipient age correlated with an increased risk for GIF on the one-yr biopsy.

Decline in native renal function early after bladder-drained pancreas transplantation alone.

BACKGROUND: Pancreas transplant alone (PTA) has become accepted therapy for select nonuremic patients with type 1 diabetes mellitus. However, PTA may lead to significant complications including a decline in native renal function. This study examines trends in native renal function during the first posttransplant year in PTA recipients with a spectrum of pretransplant glomerular filtration rates (GFR). METHODS: Renal function was studied in 23 recipients of bladder-drained PTA who underwent transplantation from April 1998 through September 2001. GFR was measured by corrected iothalamate clearance at the time of transplant evaluation and 1 year posttransplant and also calculated using the Cockcroft-Gault method at the transplant evaluation; at the day of transplantation; and at 1, 6, and 12 months posttransplant. RESULTS: Iothalamate clearance decreased in the first year in 96% of patients (22 of 23). The mean measured GFR decreased from 84 +/- 33 mL/min/1.73 m2 pretransplant to 52 +/- 26 mL/min/1.73 m2 at 1 year (P <0.001). Calculated creatinine clearance declined in the majority of patients at both 1 and 12 months after PTA, but some patients, including a few with low GFR, maintained stable renal function. Calculated GFR generally correlated well with measured GFR in most patients, with a few notable exceptions. One patient (baseline GFR, 42 mL/min/1.73 m2) developed renal failure in the first year after transplant and required kidney transplantation. CONCLUSIONS: Bladder-drained PTA results in a decline in native renal function in the majority of patients regardless of the pretransplant GFR. These data suggest the need for strategies to prevent or minimize the decline in renal function after PTA.