Hemodialysis vascular access: variable thrombus-free survival in three subpopulations of black patients.

Hemodialysis vascular access-related problems account for most hospitalizations in chronic hemodialysis patients. Although some co-morbid risk factors for early fistula failures have been described, a great deal of unknown exists as to why access survival is favorable in some patients. In this longitudinal study, fistulae patency and thrombosis episodes were monitored from placement date in three groups of end-stage renal disease (ESRD) patients who have been on dialysis for > or =90 days. Thirty-six patients (29 male; 80%) with a mean age of 42+/-2 years were monitored. The groups consisted of eight patients with biopsy-confirmed focal segmental glomeruloscierosis (FSGS), 13 with acquired immunodeficiency syndrome-related nephropathy (human immunodeficiency virus [HIV]), and 15 with hypertensive ESRD (hypertensive nephrosclerosis [HTN]) who served as controls. Diabetics and patients aged > or =64 years were excluded. Twenty-five of 36 (69%) fistulae were prosthetic (AVG), while 11 (31%) were native (AVF). The FSGS group was more likely to have an AVG (87.5%), while 54% of the HIV group had an AVG. The thrombosis event rate was significantly greater among the FSGS patients (3/patient-year) than the HIV (0.15/patient-year) and HTN (0.5/patient-year) patients (P < 0.0001 and P < 0.002, respectively). The mean thrombosis-free duration for both AVG and AVF among the HIV and HTN groups were 318.5+/-17 days and 311.7+/-22.5 days, respectively. These were significantly greater than in the FSGS group (26.5+/-7 days; P < 0.0001). The cumulative 1-year patency rate for AVG among the HIV and HTN groups was 85% and 65%, respectively, while that of the FSGS group was 0%. Kaplan-Meier hazard analysis showed that all groups were at risk of access thrombosis as time progressed, but the FSGS group had the highest risk of access thrombosis, which began from the date of placement and increased exponentially with time. The increased thrombosis rate among the patients in the FSGS group correlated with their weight (R = 0.8, P = 0.003) and pre-ESRD 24-hour urinary protein excretion (R = 0.9, P = 0.001). The HIV status appeared to confer enhanced hemodialysis access survival. This may be related to the high rate of native fistulae placement and favorable vascular reactivity to shear stress. Accelerated atherosclerosis and small caliber vessels may be responsible for the poor fistulae outcome among the FSGS group. More studies will be necessary to further explore these findings.

Successful cyclophosphamide treatment of cryoglobulinemic membranoproliferative glomerulonephritis associated with hepatitis C virus infection.

A 54-year-old man with cryoglobulinemia and chronic hepatitis C infection presented with progressive renal insufficiency caused by membranoproliferative glomerulonephritis. Because of a steady decline in renal function, cyclophosphamide therapy was instituted. Within 1 month of starting therapy, his cryoglobulins disappeared, and in 3 months, his creatinine clearance had improved from 56 mL/min to 89 mL/min. At no point in his course was there clinical evidence of liver disease. After 1 year, cyclophosphamide was successfully stopped. Fourteen months later, his creatinine clearance is 105 mL/min. These results suggest that cyclophosphamide may be useful therapy for patients with cryoglobulinemic membranoproliferative glomerulonephritis and hepatitis C virus infection who have progressive renal insufficiency.

Occupational bladder cancer in textile dyeing and printing workers: six cases and their significance for screening programs.

Occupational bladder cancer due to aniline dye intermediates such as beta-naphthylamine and benzidine has long been known; benzidine congeners (o-tolidine and o-dianisidine) are highly suspect. Among 400 men from the Amalgamated Clothing and Textile Workers Union (ACTWU) Dyers locals in New York and New Jersey screened over a 4-year period, two cases of bladder cancer were detected. (Microscopic hematuria, not cytological evaluation, prompted further investigation.) Before a 1984 ACTWU screening program in North Carolina, three workers from the same plant self-reported bladder cancers. Another member, with inconclusive screening results, was diagnosed 2 years later. For these six cases, the mean age at detection was 56.5 years (age range, 38 to 79 years), a decade earlier than age at diagnosis of nonoccupational bladder cancer in men. The average latency from onset of exposure to diagnosis was 23.3 years. These cancers provide evidence to support the initiation of screening programs for high-risk workers. To overcome the emotional and economic disincentives faced by potential victims of occupational bladder cancer, training programs are needed. Worker involvement is required, through trade union representation where possible, to assure reliable training and the equitable distribution of screening and treatment costs.

Amplification of the c-myb oncogene in a case of human acute myelogenous leukemia.

Amplification is one of the mechanisms by which cellular oncogenes may be altered in their function, possibly leading to neoplastic transformation. The oncogenes c-myc, c- abl , and c-Ki-ras are amplified in several different human neoplasias. The oncogene c-myb, which is specifically expressed and regulated in hematopoietic cells, was found to be amplified in cell lines ML-1, ML-2, and ML-3, which were separately cultured from cells of a patient with acute myelogenous leukemia (AML). A five- to tenfold amplification was correlated with high levels of expression of normal size c-myb messenger RNA and with chromosomal abnormalities in the region 6q22 -24, where the c-myb locus is normally located. Amplification and cytogenetic abnormalities were detected in DNA's from primary and secondary cultures of ML cells, suggesting that they may have contributed to leukemogenesis. The similar AML cell lines HL-60 and ML's contain different amplified oncogenes: c-myc and c-myb, respectively. Alternative activation of structurally and possibly functionally similar oncogenes may distinguish--at the pathogenetic level--phenotypically similar tumors.