| Autor: |
Chan, James C M, Grushkin, Carl M, Malekzadeh, Mohammad, Better, Ori, Fine, Richard N |
| Zdroj: |
Pediatric Research; August 1973, Vol. 7 Issue: 8 p712-718, 7p |
| Abstrakt: |
Extract: The compensatory growth of the single and transplanted kidney is demonstrated by the improvement of glomerular filtration rate (GFR) of the single kidney to achieve 50–90% of the normal value. The compensatory renal tubular acid excretion is also studied. It is clearly demonstrated that in response to a standard ammonium chloride load (75 mEq/m2) systemic acidosis (tCO2< 16 mEq/liter) occurs uniformly at 300–400 min but maximal renal acid excretion (98 ± 12 and 76 ± 17 µEq/min/1.73 m2) occurs in the normal and single kidney subjects, respectively, at 300–400 min, whereas, for the transplant subjects, maximal acidifications of 72 ± 34 and 74 ± 26 µEq/min/1.73 m2are achieved at 800 and 1,400 min for live-related and cadaveric allografts, respectively. The slower and suboptimal renal response accounts for the persistence of metabolic acidosis in the transplant population.The studies document that the important limiting factor is the reduction in glomerular filtration rate in the transplant subjects. When the low net acid excretion in the two transplant groups are factored by GFR, they become comparable with the control (donor) group as well as the normal group (P > 0.95), i.e., each remaining nephron is excreting acid normally (or supernormally) and is supportive of the “intact nephron” hypothesis.The data show a marked difference in urinary pH during acidosis between the two transplant groups: 50% of the cadaveric allografts have an inability to lower urine pH below 5.4 compared with 10% only of the live-related allografts which show such a defect. This would imply that cadaver allografts are more susceptible to an acute acid load.Speculation: The ischemia sustained at the time of transplantation results in acute tubular damage and proportionate lowering of the glomerular filtration rate which account for the impaired acidification capacity in the kidney allografts. It is also possible that circulatory damage to the glomeruli may occur in the transplantation process. It is even possible that intrarenal circulation may be altered by either transplantation or nephrectomy; although, admittedly, this last possibility seems quite unlikely. It is open to speculation what effect the age difference between the donors and the recipients may have on their different responses to acute metabolic acidosis. |
| Databáze: |
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