Little attention had been paid to J renin in clinical renal infarction until recently when we found a transient elevation of plasma renin activity (PRA) after attacks in three patients.1
We have had two additional experiences with renal infarction in a patient with a mitral prosthetic valve. The case is significant because (1) an isozyme analysis, which is generally thought to be most useful in organ diagnosis, did not help because of the multiple sources of an increased level of serum lactic dehydrogenase (SLDH) possibly involved. Here, the determination of PRA was useful and thus proved to be superior as a diagnostic aid in renal infarction. (2) This case provided an opportunity to observe the time course of the elevation of PRA along with that of the other serum enzymes, and offered a clue to the mechanism of renin release in this condition.
A 21-year-old woman has