THE ABILITY OF NEPHRITIC PATIENTS TO DEAMINIZE AND FORM UREA FROM INGESTED GLYCINE

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Abstract
In a test of the deaminizing and urea-forming functions described the plasma amino N curve and the amt. of urea formed are observed during 3 hrs. after ingestion of 25 gm. of glycine. In uremic patients the increase in plasma amino N was 2-4 times greater than in normal persons, and the return to pre-ingestion level was slower. Normal persons transformed an av. of 48% of the ingested amino N into urea N during the first 3 hrs. following the glycine. In 2 of the 3 uremic patients studied, the urea formation in this period was reduced to 10 and 24% respectively of the ingested N; but during the period 3-6 hrs. after ingestion the uremic subjects formed as much urea as the normal subjects or more. The same patients who showed high and prolonged curves for blood amino N and initially retarded urea formation after ingestion of glycine, were able to form urea from ingested ammonium citrate as rapidly as the normal persons. The curve for blood ammonia following ingestion of 13.3 gm. of ammonium citrate likewise showed no difference from the curve obtained in normal subjects. The conversion of ammonia into urea is therefore unimpaired in uremia. The retarded formation of urea observed after feeding of glycine appears to be attributable to delay in de-aminization rather than to delay in the subsequent trans-formation of the ammonia into urea. In nephritic patients in whom the nephrotic syndrome was the outstanding feature of the disease, no abnormality in the curve for plasma amino N or in urea formation was found after feeding of glycine. The finding of abnormally high curves for plasma amino N after ingestion of glycine, or even of moderately elevated content of plasma amino N in the fasting condition, does not apparently suffice to indicate the necessity for restricting protein intake.

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