Erythrocytosis was seen in two men during maintenance hemodialysis therapy for end-stage renal disease secondary to apparent chronic glomerulonephritis. Nonrenal causes of erythrocytosis such as polycythemia vera, chronic hypoxemia, high-oxygen affinity hemoglobin, and hepatoma were excluded by appropriate clinical studies. A computed tomographic scan of the abdomen showed numerous renal cysts in each patient consistent with acquired cystic disease of end-stage kidneys. Peripheral serum erythropoietin levels were elevated as measured by sensitive radioimmunoassay. The findings suggest that the erythrocytosis is caused by an erythropoietic mechanism related to the diseased kidneys. A review of the literature failed to show previous reports of this clinical association.

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Spontaneous and phytohemagglutinin (PHA)-induced lymphocyte blastogenesis (LB) was measured by the incorporation of ³H-thymidine into lymphocytes from zinc-treated (group I) and non-zinc-treated (group II) patients on maintenance hemodialysis and from normal controls. The results were expressed as disintegrations per minute (dpm) per 200,000 cells. Spontaneous LB was comparable in the 3 groups. LB in response to PHA was impaired in group II (mean dpm 28,244 ± 13,499 SEM) as compared to group I (163,407 ± 14,325; p < 0.001) or controls (193,711 ± 9,406 ;p < 0.001). In 5 group II patients the mean dpm rose from (45,630 ± 26,334 SD to 211,795 ± 78,231; p < 0.025) after zinc therapy. The mean percentages of viable lymphocytes after 72 h of culture were 53.8,85.8 and 85.5 in groups II, I, and controls, respectively. These results clearly indicate that zinc therapy improves lymphocyte function and viability in uremia and suggest that abnormal zinc metabolism may play a role in the impaired cellular immunity in this disorder.

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Urinary excretion of zinc, sodium, potassium, and calcium was studied in anesthetized dogs under conditions of volume expansion by saline infusion and volume expansion plus chlorothiazide administration. Zinc excretion was positively correlated to the fractional water excretion, as well as to th excretion of the other cations, during volume expansion. Chlorothiazide administration during volume expansion increased the zinc, sodium, and potassium excretion without changing that of calcium. The enhanced zinc excretion during chlorothiazide diuresis was equal to that expected on the basis of the increase in fractional water excretion alone. The urinary concentration of zinc appeared inversely related to the urine flow rate, reaching a minimum below that of the plasma ultrafilterable zinc concentration. The ratio of the clearance of zinc to that of sodium was 0.28, indicating a greater degree of net reabsorption for zinc than for calcium. These findings suggest that zinc and sodium reabsorption may be inhibited to a similar degree at chlorothiazide-sensitive sites in the tubule. Furthermore, the zinc reabsorptive mechanism seems capable of lowering urinary zinc concentration below that of ultrafiltrate and appears related in some way to sodium reabsorption.