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We prospectively studied the in vivo dialytic clearance of iron after deferoxamine (DFO) administration in four stable iron-overloaded chronic hemodialysis patients by quantifying iron concentration in blood entering and leaving the dialyzer and in dialysate after infusions of DFO. No significant arteriovenous iron differences were demonstrated. The mean ratio of venous to arterial iron approached identity at 1.005. All dialysate concentrates used contained large amounts of iron (300–610 μg/dl). No changes in efferent versus afferent dialysate iron concentration could be demonstrated. We conclude (a) iron removal during dialysis with DFO was not demonstrated; (b) the dialysate concentrate tested contained large amounts of iron; (c) in view of potentially significant toxicity, and lack of demonstrable therapeutic benefit, caution in prescribing DFO chelation therapy for iron overload is recommended.

1. The daily rate of urea nitrogen and creatinine production was determined in 7 patients with chronic stable azotemia and 3 normal subjects, maintained on a reduced protein intake. In addition, the effect of hemodialysis on urea nitrogen and creatinine production was observed in all the azo-temic patients. 2. In 7 cases predialysis urea nitrogen production was similar to that found in normal subjects and averaged 55% of the nitrogen intake. In 2 cases urea nitrogen production was elevated, being equal to or exceeding the dietary nitrogen. The rate of creatinine production in the azotemic patients was slightly lower than that found in normal subjects. 3. Postdialysis urea nitrogen production increased significantly in 5 cases whose predialysis PUN ranged from 42 to 73 mg%, and decreased in 4 cases with predialysis PUN of 87 to 192 mg%. Creatinine production decreased in all but one case.

The effects of renin infusion were studied in anesthetized normal and buffer-nerve sectioned dogs during osmotic (mannitol) diuresis and hydropenia. Renin produced a rise in blood pressure and a decrease in CPAH. These changes were more marked in buffer-nerve sectioned dogs. CMfell by an average of 15% in 6 normal dogs in which urine and salt excretion also decreased. However, in another 4 normal dogs in which CMremained unchanged during renin infusion, water and salt excretion increased moderately. In all the buffer-nerve sectioned dogs renin caused significant diuresis and natriuresis although CMdecreased slightly. The results show that buffer-nerve sectioned dogs are more sensitive than normal dogs to the diuretic action of renin. The possible mechanisms of this action have been discussed.

Angiotensin II was administered at rates of 0.3 to 0.6 μg per minute over 6 to 24 hours to 6 subjects with hypertension of various etiologies under conditions of positive and negative sodium balance. Angiotensin produced hypernatriuresis under condition of positive sodium balance. The effect was most marked in those subjects having a diastolic blood pressure above 110 mm Hg.Miss S. Goodman, Mrs. S. Beacher and Miss M. E. Novotny provided technical assistance. Angiotensin II (Hypertensin Ciba) and aldosterone (d-aldosterone Ciba) were obtained through the courtesy of Dr. W. E. Wagner, Summit, N. J.

In the course of the past 15 years, dialysis has been employed with increasing frequency for treating patients with chronic renal failure. Acknowledged indications for dialysis include rapid deterioration caused by an intercurrent illness or acute exacerbation of the underlying disease, and relief of azotemia before surgery.1-3 More recently, dialysis has been employed in the management of patients with end-stage kidney disease.4,5 A significant prolongation of life has been obtained in a few patients by a program of "periodic" dialyses performed at intervals of three to seven days.6 Unfortunately, this type of therapy has so many drawbacks and is so costly that it can be made available to a very small minority of carefully selected patients.An alternate approach to the therapy of advanced, chronic renal failure is to employ dialysis on an "intermittent" basis, whenever medical management alone fails to produce relief of uremia. The present

Angiotensin II (valine-5 angiotensin II amide) and pitressin were administered intravenously during mannitol and water diuresis to subjects with diabetes insipidus. Angiotensin II in doses of 0.0025 to 0.0050 μg per kg per minute caused a small but definite increase in blood pressure in 5 of 7 experiments, a decrease in endogenous creatinine clearance of about 11%, and a decrease in urine flow and water clearance of about 40%. The rate of sodium excretion was depressed by nearly 50%, while that of potassium decreased much less. Pitressin produced changes of water excretion qualitatively similar to those caused by angiotensin II. However, this effect was achieved without alteration in blood pressure, although filtration rate decreased. Further, pitressin did not consistently affect excretion of sodium and potassium. The results suggest that angiotensin II at the dose-ranges examined inhibits water and salt excretion by direct tubular action.