Enzymes in renal diseases.

Recent progress is reviewed in the diagnostic enzymology of renal dis­ eases. Enzyme determinations in blood serum are of little value. Activity increases during hemodialysis are most likely due to fluid redistribution. Enzymes are transported from the interstitium via the lymph into the intravasal space where they accumulate. Determination in the urine of enzymes of the brushborder of the proxi­ mal convoluted tubules (e.g., alanine aminopeptidases) and lysosomal en­ zymes (e.g., ^-glucuronidase) aid in the recognition and differential diag­ nosis of renal diseases. A pattern consisting of alanine aminopeptidase, /3-glucuronidase, lysozyme and protein appears to be of particular value. A recently proposed working hypothesis links enzymuria to the reabsorp­ tion in the nephron of lysosomotropic agents, including protein. Enzyme activity changes in the renal cortex during the acute rejection of kidney transplants in the cat suggest that the kidney loses its potential for fatty acid oxidation, citrate cycle, gluconeogenesis and amino acid trans­ amination and deamination. The potential for glycolysis and hexose mono­ phosphate shunt is maintained. Rejected human kidney transplants show a similar enzyme pattern. More research is necessary before enzyme deter­ minations in renal tissue may be recommended as aids in assessment of the viability of a renal transplant or a conserved kidney prior to transplantation. In this review of diagnostic enzymology in renal diseases which is lim­ ited to more recent perceptions, the subject is divided into three parts: (1) enzymes in blood plasma; (2) enzymes in urine; (3) enzymes in renal tissue. Enzymes in Blood Plasma It appears as if diagnostic enzymology in blood plasma offers little in the recog­ nition and differential diagnosis of renal diseases, with the exception perhaps of the renal infarct.1,3,30,34 422 However, some recent observations are worth to be mentioned on enzyme activ­ ity changes in the serum in chronic renal failure treated with hemodialysis. In 1968 Ringoire reported that LDH-5 (M4) increases in serum directly following hemodialysis.25 He believed that this ENZYMES IN RENAL DISEASE 423 isoenzyme originated from the diseased kidneys,* despite the fact that human kidney contains comparatively little LDH-5.20 Enzyme activity changes in serum during hemodialysis were reinves­ tigated in this laboratory, and the scope was broadened to include 11 enzymes, f AlAT, ALD, AspAT, GGTP, GLDH, G-6-PD, LAP, LDH, MDH, PGDH and SDH were determined in 16 patients over a period of about one year. The total number of dialyses were 82, varying from 1 to 14 for each patient.10 Frequency and direction of the activity changes are shown in figure 1. The con­ siderable differences must be noted which were found between the enzymes. In figure 2 are shown the plotted means of the activities before and after hemodialysis. The changes were statisti­ cally significant except for G-6-PDH and PGDH. Again, the differences must be noted between the relative extent of the activity elevations. The mean increase for MDH was about 58 percent as compared to 25 percent for AspAT and less than 10 percent for LAP. The results rule out simple hemoconcentration as the cause for enzyme activ­ ity increases, as has been found in the acute decrease of the plasma volume.11 Blood cells, which are exposed to a con­ siderable mechanical stress during % lOOn 80> S) 2i 60 k Ï 2 40-