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Titolo:
Renal tubular peptide catabolism in chronic vascular rejection
Autore:
Rustom, R; Grime, JS; Sells, RA; Amara, A; Jackson, MJ; Shenkin, A; Maltby, P; Smith, L; Hammad, A; Brown, M; Bone, JM;
Indirizzi:
Univ Liverpool, Dept Med, Cellular Pathophysiol Grp,Clin Dept, Sir Peter Medawar Reg Renal Transplant Unit, Liverpool, Merseyside, England Univ Liverpool Liverpool Merseyside England verpool, Merseyside, England
Titolo Testata:
RENAL FAILURE
fascicolo: 3-4, volume: 23, anno: 2001,
pagine: 517 - 531
SICI:
0886-022X(2001)23:3-4<517:RTPCIC>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
RADIOLABELED APROTININ TRASYLOL; CONVERTING ENZYME-INHIBITION; ANGIOTENSIN-II; PROTEINURIA; THERAPY; PROGRESSION; METABOLISM; FAILURE; KIDNEY; AMMONIAGENESIS;
Keywords:
lisinopril; chronic vascular rejection; proteinuria; proximal tubular peptide hypercatabolism; ammonia; acidosis; NAG; aprotinin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Rustom, R Univ Liverpool, Dept Med, Cellular Pathophysiol Grp,Clin Dept, Sir Peter Medawar Reg Renal Transplant Unit, Liverpool, Merseyside, England Univ Liverpool Liverpool Merseyside England erseyside, England
Citazione:
R. Rustom et al., "Renal tubular peptide catabolism in chronic vascular rejection", RENAL FAIL, 23(3-4), 2001, pp. 517-531

Abstract

Chronic vascular rejection (CR) is the commonest cause of renal transplantloss, with few clues to etiology, but proteinuria is a common feature. In diseased native kidneys, proteinuria and progression to failure are linked. We proposed a pathogenic role for this excess protein at a tubular level in kidney diseases of dissimilar origin. We demonstrated in both nephrotic patients with normal function and in those with failing kidneys increased renal tubular catabolism and turnover rates of a peptide marker, Aprotinin (Apr), linked to increased ammonia excretion and tubular injury. These potentially injurious processes were suppressed by reducing proteinuria with Lisinopril. Do similar mechanisms of renal injury and such a linkage also occurin proteinuric transplanted patients with CR, and if so, is Lisinopril then of beneficial value? We now examine these aspects in 11 patients with moderate/severe renal impairment ((51)CrEDTA clearance 26.2 +/- 3.3 mL/min/1.73 m(2)), proteinuria (6.1 +/- 1.5 g/24 h) and biopsy proven CR. Lisinopril (10-40 mg) was given daily for 2 months in 7 patients. Four others were given oral sodium bicarbonate (Na HCO3) for 2 months before adding Lisinopril. Renal tubular catabolism of intravenous Tc-99m-Apr (Apr* 0.5 mg, 80 MBq), was measured before and after Lisinopril by gamma -ray renal imaging and urinary radioactivity of the free radiolabel over 26 h. Fractional degradation was calculated from these data. Total 24 h urinary N-acetyl-beta -glucoaminidase (NAG) and ammonia excretion in fresh timed urine collections were also measured every two weeks from two months before treatment. After Lisinopril proteinuria fell significantly (from 7.8 +/- 2.2 to 3.4 +/- 1.9 g/24 h, p < 0.05). This was associated with a reduction in metabolism of Apr* over 26 h (from 0.5 +/- 0.05 to 0.3 +/- 0.005% dose/h, p < 0.02), and in fractional degradation (from 0.04 +/- 0.009 to 0.02 +/- 0.005/h, p < 0.01). Urinary ammonia fell, but surprisingly not significantly and this was explainedby the increased clinical acidosis after Lisinopril, (plasma bicarbonate fell from 19.1 +/- 0.7 to 17.4 +/- 0.8 mmol/L, p < 0.01), an original observation. Total urinary NAG did fall significantly from a median of 2108 (range 1044-3816) to 1008 (76-2147) mu mol/L, p < 0.05. There was no significantchange in blood pressure or in measurements of glomerular hemodynamics. Inthe 4 patients who were given Na HCO3 before adding Lisinopril, both acidosis (and hyperkalemia) were reversed and neither recurred after adding Lisinopril. These observations in proteinuric transplanted patients after Lisinopril treatment have not been previously described.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 04:27:32