title: Renal functional reserve in kidney and heart transplant recipients.
abstract: Renal functional impairment paradoxically often seems less severe in kidney than in heart-transplant recipients (KTR and HTR, respectively) when both are submitted to cyclosporine therapy. Renal functional reserve (RFR), elicited by a 3-h intravenous amino acid infusion, was examined in 12 KTR and 13 HTR at 7 to 8 months, appropriately compared with either eight one-kidney or 12 two-kidney healthy control subjects (1K.C and 2K.C, respectively). Baseline GFR was 54 +/- 4 mL/min in KTR and 71 +/- 4 mL/min in HTR (P < 0.05). During amino acid infusion, the maximum increase in GFR (which represented RFR) was 17 +/- 3 mL/min in both KTR and HTR (P < 0.001). RFR in KTR was 96 +/- 18% of that in 1K.C, whereas RFR in HTR was only 59 +/- 9% of that in 2K.C. Effective RPF increased (41 +/- 8 mL/min, P < 0.001), and renal vascular resistances decreased (48 +/- 17 mm Hg/L per min, P < 0.05) in KTR but not in HTR. These results demonstrate that both KTR and HTR possess a renal reserve but that the single renal graft in KTR retains a proportionally higher baseline GFR and a better ability to exhibit a RFR than the two native kidneys in HTR. This dissimilar impairment could result from slightly higher cyclosporine dosage, activation of the intact renal sympathetic innervation accentuated by cardiac denervation, renal consequences of former heart failure and potential alterations in the cardiac graft function, and/or higher prevalence of hypertension and additive therapies in HTR.
authors.affiliation: Laboratoire Explorations Fanctionnelles Rénales, Ranguell University Hospital, Toulouse, France.
authors.forename: J L
authors.initials: JL
authors.lastname: Ader
authors.forename: I
authors.initials: I
authors.lastname: Tack
authors.forename: D
authors.initials: D
authors.lastname: Durand
authors.forename: T
authors.initials: T
authors.lastname: Tran-Van
authors.forename: L
authors.initials: L
authors.lastname: Rostaing
authors.forename: J M
authors.initials: JM
authors.lastname: Suc
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood; D000596:Amino Acids; D001379:Azathioprine / Q000627:therapeutic use; D003404:Creatinine / Q000097:blood; D016572:Cyclosporine / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D005260:Female; D005919:Glomerular Filtration Rate; D016027:Heart Transplantation / Q000502:physiology*; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000453:epidemiology / Q000503:physiopathology; D007166:Immunosuppressive Agents / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use; D007444:Inulin; D007668:Kidney / Q000187:drug effects / Q000294:innervation / Q000503:physiopathology*; D016030:Kidney Transplantation / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use; D012083:Renin / Q000097:blood; D013564:Sympathetic Nervous System / Q000503:physiopathology; D010130:p-Aminohippuric Acid
chemical_list: D000596:Amino Acids; D007166:Immunosuppressive Agents; D000450:Aldosterone; D016572:Cyclosporine; D007444:Inulin; D003404:Creatinine; D012083:Renin; D001379:Azathioprine; D011241:Prednisone; D010130:p-Aminohippuric Acid