Lipoprotein lipid abnormalities in healthy renal transplant recipients: persistence of low HDL2 cholesterol.

There is disagreement about the prevalence and character of lipoprotein lipid abnormalities in renal transplant patients. To test the hypothesis that these abnormalities may be related to the coexistence of medical conditions and medications which affect lipoprotein metabolism in these patients, triglyceride (TG), cholesterol (C), high-density lipoprotein (HDL) and HDL-C subfractions were measured in 26 transplanted patients (10 F/16 M), control subjects matched for age, sex, weight and race and uremic patients being treated with hemodialysis. Female transplant recipients had higher TG (181 +/- 47 vs. 68 +/- 6 mg/dl; p less than 0.001), C (242 +/- 19 vs. 165 +/- 9 mg/dl; p less than 0.01), and low-density lipoprotein (LDL)-C (155 +/- 15 vs. 93 +/- 8 mg/dl; p less than 0.01) than controls. Levels of HDL-C were similar, but HDL2 was significantly lower in the transplanted patients (9 +/- 2 vs. 19 +/- 2 mg/dl; p less than 0.01). Compared to the uremic patients, female transplanted patients had higher C (242 +/- 19 vs. 178 +/- 22 mg/dl; p less than 0.01), LDL-C (155 +/- 15 vs. 94 +/- 18 mg/dl; p less than 0.01), HDL-C (51 +/- 5 vs. 32 +/- 4 mg/dl; p less than 0.001) and HDL3-C (42 +/- 4 vs. 26 +/- 2 mg/dl; p less than 0.001); however, HDL2-C levels were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

A case of agnogenic myeloid metaplasia evolving into acute myelogenous leukemia associated with the development of trisomy 11 in bone marrow cells.

An 83-year-old woman who had a 5-year history of agnogenic myeloid metaplasia and a previous normal marrow cell karyotype presented with acute myelogenous leukemia (AML) associated with the development of trisomy 11 in 100% of cultured marrow cells. Isolated trisomy 11 in marrow cells has been reported previously in five cases of AML, suggesting that trisomy 11 is a nonrandom chromosomal aberration associated with AML.

Characteristics of early routine renal allograft biopsies.

The assumption that renal allograft histology should be perfectly normal during quiescence in the absence of rejection or nephrotoxic insults has not been adequately investigated. To study this, routine renal allograft biopsies were performed at approximately 1 and 4 weeks, when patients often had normal function or stable acute tubular necrosis (ATN). These were compared with biopsies from other patients during autologous ATN or clinically evident allograft rejection. There were two new findings: (1) Almost all biopsies contained an interstitial infiltrate, so that only the presence of vasculitis provided a clear distinction between rejection and quiescence. Most of the biopsies with infiltrates were from patients who had never received cyclosporine, so that an infiltrate does not necessarily signify toxicity due to this drug. (2) A major proportion of the cells in some biopsies appeared to express both the helper/inducer and the cytotoxic/suppressor phenotype, and a similar finding after in vitro stimulation suggests that this represents a cell population that is activated in some way.

Interstitial nephritis, proteinuria, and renal failure caused by nonsteroidal anti-inflammatory drugs. Immunologic characterization of the inflammatory infiltrate.

Nine patients with the unusual combination of renal failure, nephrotic-range proteinuria, and biopsy-proved interstitial nephritis are described. Six of these patients had received nonsteroidal anti-inflammatory agents (three fenoprofen, one ibuprofen, one zomepirac, and one tolmetin). The remaining three patients had no history of exposure to drugs known to cause interstitial nephritis. Immunologic characterization of the infiltrating cells with monoclonal antibodies showed that the majority of cells in most cases were cytotoxic T cells, although some B cells were present in all cases. Giant collecting duct cells were seen in half the patients with drug exposure but in none of the others. Otherwise, there were no conspicuous morphologic differences between patients with and without drug exposure. Many of the patients had associated glomerular abnormalities. Only the zomepirac and tolmetin recipients showed pure interstitial disease. The three fenoprofen recipients and the zomepirac and tolmetin recipients regained normal renal function after the drug was discontinued. The combination of renal failure, nephrotic range proteinuria, and interstitial nephritis is one form of nephrotoxicity observed in patients treated with nonsteroidal anti-inflammatory agents. However, this lesion, which may be mediated by cytotoxic T cells, may also be seen rarely in patients with no apparent drug exposure.

An approach to the control of massive hemorrhage in cyclophosphamide-induced cystitis by intravenous vasopressin: a case report.

Massive bleeding owing to cyclophosphamide-induced hemorrhagic cystitis was not affected by intravesical instillation of 4 per cent formalin or 1 per cent silver nitrate. After initiation of a continuous systemic infusion of vasopressin hematuria and transfusion requirements diminished markedly. Adverse reactions were mild. Intravenous vasopressin was a safe and effective means to control temporarily life-threatening hemorrhagic cystitis.