Introduzione: l’incidenza e le cause di insufficienza renale in pazienti in NPD per IICB non sono ancora chiare. Questo studio si è prefisso di valutarle.
Materiali e metodi: studio prospettico di 30 mesi condotto in pazienti adulti. funzione renale valutata tramite filtrato glomerulare(eGFR) secondo MDRD(Modification of Diet in Renal Disease), cistatina C. eGFR< 60 ml è stato considerato diagnostico per IRC.
Parametri valutati: caratteristiche dell'insufficienza intestinale e programma di NPD, infezioni del catetere venoso centrale (CRBSI).
Risultati: 53 hanno terminato il follow-up a 30 mesi e sono stati quindi inclusi nell’analisi statistica. i pazienti sono stati suddivisi in 3 gruppi in base al eGFR: Gruppo A(n.12) pazienti con IRC al baseline, e Gruppo B (N.6) pazienti che sviluppano IRC durante follow up, Gruppo C (n.35) pazienti che mantengono eGFR ≥ 60 ml/min.
Conclusioni: durante un follow up di 30 mesi, il 14.6% dei pazienti in NPD ha sviluppato una IRC. La frequenza di CRBSI si è confermata essere un fattore di rischio per la IRC, mentre il volume sembrerebbe avere un ruolo protettivo.Objective: The incidence and causes of chronic renal failure(CRF) in patients on home parenteral nutrition(HPN) remain to be clarified. We investigated renal function outcome in patients on long term HPN for chronic intestinal failure(CIF) due to benign disease.
Research Methods & Procedures: A 30 month prospective study was performed on adult patients on HPN at 31/10/2011(baseline). Renal function was evaluated by: estimated glomerular filtration rate (eGFR) according to MDRD(Modification of Diet in Renal Disease) and by serum Cystatin C. eGFR< 60 ml was considered indicative of CRF.
Parameters evaluated: characteristics of CIF and HPN program; catheter related bloodstream infection(CRBSI) episodes.
Statistic: patients who completed follow up(Fup) period were included in the analysis; non parametric tests.
Results: Fifty-three patients were analyzed: 39 short bowel syndrome, 12 chronic intestinal pseudo obstruction, 2 mucosal disease. According to the eGFR at baseline and to its outcome during the Fup, patients were categorized in 3 groups: A) presence of CRF at baseline(n. 12) ; B) development of CRF during Fup(n. 6); C) normal eGFR at both baseline and Fup(n. 35). During Fup, the variation of eGFR was -5.87%/year in group A, -12.75% in B and +1.19 in C(p=0.001). At the end of Fup, Cystatin C was higher in group A than in C(p=0.001). The highest incidence of CRBSI (episodes/year) was observed in group B(p=0.005). The median of the daily volume(ml) of HPN was 1339 in group A, 589 in B and 1960 in C (p=0.202; p=0.082 between B and C).
Conclusions: Along a 30 month period, a CRF developed in about 15% of patients on long term HPN. The CRBSI appear a risk factor. The volume of HPN infusion may be a protective factor