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C E Kew

Publications and source records attributed to C E Kew.

4 recordsLinked to original sources

Postransplant lymphoproliferative disorder localized near the allograft in renal transplantation.

BACKGROUND: Posttransplant lymphoproliferative disorder (PTLD), a complication of immunosuppression, develops in approximately 1% of renal allograft recipients. Typically, PTLD is a proliferation of B-cells associated with Epstein-Barr virus (EBV) infection; it is said to be most often a systemic disease. Involvement occasionally is localized near the allograft. METHODS: This is a retrospective analysis of all cases of PTLD in recipients of 1474 renal transplants performed at University of Alabama at Birmingham between 1993 and 1997. RESULTS: Of 14 patients developing PTLD, 10 had disease localized near the allograft. The mean interval from transplantation to diagnosis was 221 +/- 70 days. All patients presented with renal dysfunction; an ultrasound examination revealed a hilar mass, with hydronephrosis in five and stenosis of renal vessels in eight. No patient had lymphadenopathy, according to computerized tomographic or magnetic resonance imaging findings. After reduction of immunosuppressive therapy, seven required a nephrectomy because of rejection, progressive dysfunction, or mass enlargement. Tissue recovered in four patients was consistent with PTLD; the tumors in the remaining three patients were unresectable and regressed. One patient died 1 month after a nephrectomy, and another died 4 years after surgery; neither had evidence of PTLD when they died. Three patients retain functional grafts without clinical or radiographical evidence of progression. All patients with disseminated disease died. CONCLUSIONS: In a large cohort of renal allograft recipients, PTLD affected 1%. Disease localized near the allograft was the most common variant. For most patients with localized disease, the outcome was graft loss, and the mortality was low. Localized PTLD should be considered in the differential diagnosis of allograft dysfunction in the 1st posttransplant year.

Adolescent↗

The best way to manage hypertension after renal transplantation.

Hypertension in renal allograft recipients is a common problem arising from multiple factors, including peripheral vascular damage caused by pretransplant hypertension, side effects of immunosuppressive medications, allograft dysfunction, renal artery stenosis, recurrent glomerulonephritis, synthesis of vasoconstrictive hormones by the native kidneys, and excessive dietary salt intake. Identification of modifiable factors causing hypertension and concurrent medical conditions, and measurement of glomerular filtration rate, cyclosporine/tacrolimus blood levels, and magnitude of proteinuria are essential to tailor treatment for an individual patient. Lifestyles that exacerbate hypertension should be modified. For pharmacological therapy, diuretics and calcium channel blockers are first-line agents in patients on cyclosporine shortly after transplant. Angiotensin-converting enzyme inhibitors are good choices for patients with significant proteinuria. Reduction of immunosuppression will improve hypertension in some patients, but entails a potential risk of rejection or graft loss. Angioplasty is necessary in patients with a functionally significant stenosis of the allograft renal artery. Other patients on maximal medical therapy may benefit from native nephrectomy.

Humans↗

Focal posttransplantation lymphoproliferative disorder at the renal allograft hilum.

OBJECTIVE: This report describes the imaging characteristics of focal posttransplantation lymphoproliferative disorder. CONCLUSION: Posttransplantation lymphoproliferative disorder may be limited to the allograft. A focal complex mass in the renal allograft hilum surrounding the main renal blood vessels is a common finding and can be visualized with sonography. MR imaging can help increase diagnostic confidence.

Adult↗

High flux plasma exchange using a modified rotating membrane system.

The results of increasing blood flow capability in a modified system for plasma exchange with a rotating filter are reported. There were 742 treatments performed with the authors' original system (OS), limited to blood flows of 100 ml/ min, and 327 treatments performed with the updated system (US), allowing for blood flows of 150 ml/min. Blood flows for OS were 98 +/- 5 ml/min (mean +/- SD) vs 145 +/- 12 ml/min for US (p < 0.001). Plasma flows were 65 +/- 7 ml/min for OS vs 98 +/- 12 ml/min for US (p < 0.001). Plasma removal rate was 42 +/- 8 ml/min for OS vs 61 +/- 14 ml/min for US (p < 0.001). Mean treatment time was reduced from 76 +/- 23 min for OS to 52 +/- 17 min for US (p < 0.001) in spite of providing a similar amount of plasma removed per treatment (3,113 +/- 577 ml/Rx for OS vs 3078 +/- 797 ml/Rx for US; p = 0.48). Despite statistical significance, there were only small differences in filtration fractions (65 +/- 12% for OS vs 62 +/- 11% for US; p < 0.001) and patient hematocrits (34 +/- 6% for OS vs 33 +/- 6% for US; p < 0.001). In conclusion, modification of the OS to allow for increased blood flow has resulted in a substantial improvement in procedure efficiency and a clinically useful decrease in treatment time.

Biocompatible Materials↗