An immunocytochemical study of H+ ATPase in kidney transplant rejection. J Lab Clin Med 1996 Mar;127(3):310-4
Date
03/01/1996Pubmed ID
9273365DOI
10.1016/s0022-2143(96)90100-6Scopus ID
2-s2.0-0030091638 (requires institutional sign-in at Scopus site) 16 CitationsAbstract
Kidney transplant rejection may be accompanied by defective urinary acidification. Its pathogenesis is unknown. There are shared histologic features between kidney transplant rejection and the distal renal tubular acidosis (RTA) of Sjogren syndrome, which led us to hypothesize that deficient collecting duct H+ adenosine triphosphatase (ATPase) expression--which is lacking in the RTA of Sjogren syndrome - may cause the RTA of kidney transplant rejection. Six kidney transplant recipients with biopsy evidence for rejection and two control subjects were studied physiologically and by immunohistochemistry. We found defective urinary acidification in all 6 kidney transplant patients. Ammonium excretion was diminished in relation to the degree of azotemia. There was an abnormal response to furosemide in all 6, suggesting distal tubular dysfunction. Distal H+ ATPase staining was reduced in relation to the degree of azotemia, although it was not totally absent even in the worst case. This was paralleled by the urinary PCO2 response. Both control subjects had good urine PCO2 and H+ ATPase staining and adequate urine pH response to furosemide. They had reduced urinary ammonium (NH4) concentrations in relation to modest azotemia. We conclude that kidney transplant rejection may be accompanied by defective urinary acidification, which is not primarily due to a lack of H+ ATPase. The RTA of kidney transplant rejection appears to result from defective ammonium excretion, generalized distal tubular malfunction, and--in severe cases--from a reduction in distal nephron H+ ATPase expression.
Author List
Jordan M, Cohen EP, Roza A, Adams MB, Johnson C, Gluck SL, Bastani BMESH terms used to index this publication - Major topics in bold
Acidosis, Renal TubularAmmonia
Carbon Dioxide
Furosemide
Glomerular Filtration Rate
Graft Rejection
Humans
Hydrogen-Ion Concentration
Immunohistochemistry
Kidney
Kidney Transplantation
Partial Pressure
Proton-Translocating ATPases
Staining and Labeling
Urine
