Review of a large renal transplant experience revealed a 17.3% incidence of posttransplant erythrocytosis. The influence of kidney source, pretransplant hematocrit, duration of pretransplant dialysis, renal transplant function, acute rejection, transplant renal artery stenosis, urinary tract obstruction, smoking, diabetes, retention of native kidneys, splenectomy, parathyroidectomy, immunosuppression, hypertension, and liver enzyme abnormalities on the development of erythrocytosis in 53 recipients was determined. Comparison was made with 49 control recipients matched for kidney function, time after grafting, age, and sex. Erythrocytosis occurred 3 to 90 months after transplantation and persisted for 1 to over 84 months. Risk factors for the development of erythrocytosis were smoking, diabetes, and a rejection free course. In contradistinction to previous smaller series, erythrocytosis occurred in patients with good renal function (serum creatinine 1.62 +/- 0.43 mg/dl) without prominence of graft rejection, transplant artery stenosis or obstruction. Despite therapeutic phlebotomy, 11 thromboembolic events occurred in 10 of the 53 patients with erythrocytosis, but in none of the controls (P less than 0.001). The high incidence of erythrocytosis following renal transplantation and the risk of associated thromboembolic events should encourage awareness and controlled evaluation of therapeutic modalities.

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The angiotensin antagonist [Sar1-Ile8]angiotensin II was infused into the lateral ventricles of mature spontaneously hypertensive and normotensive Wistar-Kyoto rats. Infusions were maintained at rats of 1200 ng/h for 6 days, and blood pressure was measured daily in the unanesthetized state. Blood pressure reduction occurred promptly and only in the hypertensive animals. This antihypertensive effect persisted for several days after discontinuation of the infusion. In contrast, iv infusion of the angiotensin antagonist at comparable doses failed to alter blood pressure in any significant fashion. These data suggest that the brain isorenin system participates in the maintenance of hypertension in the spontaneously hypertensive rat.

Renal cyst epithelial transport of organic molecules was investigated during three separate cyst drainage procedures in a non-uremic patient with polycystic kidney disease (PCKD). Following constant intravenous insulin infusion, four of eight sampled cysts achieved concentrations exceeding those expected by glomerular filtration alone. Likewise, cyst concentrations of the filtered radionuclide Tc DTPA were up to 3.7 times simultaneous plasma levels. Both PAH and I-131 hippuran accumulated in all cysts suggesting intact tubular secretory mechanisms. Quantitative amino acid levels in two proximal nephron cysts were identical to serum. Since concentrations of inulin, DTPA, and amino acids exceed levels expected if cystic nephrons had normal glomerular filtration and tubular reabsorptive properties, other mechanisms are likely. Simple diffusion across altered epithelial surfaces could partially account for the observed cyst concentrations of each organic molecule and, by ion trapping, contribute to progressive cyst growth in PCKD.

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