Hypercoagulability in a patient with chronic chyluria, proteinuria and hypoalbuminaemia.

We describe the case of a young man with prolonged and severe chyluria from a previous parasitic infection. He presented with an acute myocardial infarction most likely secondary to increased clotting tendency. He had a spontaneously formed blood clot in his left anterior descending coronary artery. In the setting of hypo-albuminemia (which has occurred because of obligate losses of protein from lymphuria), he has increased production of factor VIII levels and increased clotting tendency. In addition, because of obligate and unregulated fluid losses he has chronic dehydration, miscrovascular ischemia and secondary polycythemia. This polycythemia further increases his risk of hypercoagulability.

Human and murine kidneys show gender- and species-specific gene expression differences in response to injury.

The incidence of End Stage Renal Disease (ESRD) is approximately 50% higher in men than women. In order to understand the molecular basis of this gender disparity, we examined sex specific gene expression patterns in control and diseased, human and murine kidney samples. Using the Affymetrix platform we performed comprehensive gene expression analysis on 42 microdissected human kidney samples (glomeruli and tubules). We identified 67 genes with gender biased expression in healthy human kidneys and 24 transcripts in diseased male and female human kidneys. Similar analysis performed in mice using male and female control and doxorubicin induced nephrotic syndrome kidneys identified significantly larger number of differentially expressed transcripts. The majority of genes showing gender biased expression either in diseased human and murine kidneys were different from those differentially expressed in healthy kidneys. Only 9 sexually dimorphic transcripts were common to healthy human and murine kidneys and five showed differential regulation in both human and murine diseased kidneys. In humans, sex biased genes showed statistical enrichment only to sex chromosomes while in mice they were enriched to sex chromosomes and various autosomes. Thus we present a comprehensive analysis of gender biased genes in the kidney. We show that sexually dimorphic genes in the kidney show species specific regulation. Our results also indicate that male and female kidneys respond differently to injury. These studies could provide the basis for the development of new treatment strategies for men and women with kidney disease.