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The rate of change of the serum creatinine concentrations in 63 patients with chronic progressive renal disease of varied etiology was examined by linear regression analysis using the logarithm or the reciprocal of the serum creatinine concentration versus time. A single straight line was described by one or the other of these relationships in 53 patients. Six patients had an accelerated rate of nephron destruction terminally (two slopes) regardless of the mathematical analysis. The remaining four patients had course changes either due to apparent spontaneous remissions or temporally related to therapy. These data suggest that (functional) nephron loss in chronic progress disease is orderly and mathematically definable. The theoretical implications are that functional nephron loss is either exponential (log Cr) or constant (1/Cr).

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The synthesis of aminolevulinic acid (ALA) is the first in a series of enzymatic reactions leading to the formation of tetrapyrrols and heme. The reactions shown on this slide as well as the final two steps in heme synthesis are localized within mitochondria. This fact has implicated the synthesis of ALA as the site of a feedback control mechanism whereby heme synthesis may be regulated i and integrated with the formation of other parts of the hemoglobin molecule. The following studies were performed: (1) to characterize the kinetics of the synthesis iff"% O$ ALA-for enzyme obtained from chicken erythrocytes and (2) to identify and ascertain the importance of potential physiological inhibitors in controlling the rate of heme synthesis. A crude preparation of mitochondria capable of carrying out the reactions shown on this slide was obtained from reticulocytes of anemic chickens. The preparation was free of hemoglobin and enzymes utilizing ALA so that its formation could be followed. Incubations for one hour were performed at pH optimal .for ALA synthetase varying the concentration of substrate to permit construction of standard doublereciprocal Lineweaver-Burke plots. In the present studies Succinyl CoA was generated either from c(ketoglutarate or from sudcinate in the presence of optimal concentrations of cofactors for the reactions, as npted on the slide, and relying upon dKG oxidase and succinyl CoA synthetase known to be present in mitochondria of the preparation.

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