Acute effects of ciclosporin on renal hemodynamics and urinary protein excretion in patients with the nephrotic syndrome

G. Fuiano, G. Conte, V. Sepe, M. Balletta, P. Cianfrone, C. Libetta, G. Romano, M. Sabbatini, V. Bisesti

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The possibility that the renal hemodynamic abnormalities associated with ciclosporin (CS) administration are enhanced in nephrotic patients (NP), leading to severe impairment of renal function and/or to modifications in proteinuria, has not hitherto been tested. Ten NP and 8 healthy subjects (NC) were examined before and after oral CS administration (10 mg/kg body weight in NP and 12 mg/kg body weight in NC: a lower dosage was adopted in NP because of edema overestimating the actual body weight) under water diuresis by standard renal clearance methods. Basal blood volume was lower in NP. Blood CS levels were not significantly different in the two groups. Basal glomerular filtration rate (GFR) was similar in NP and NC, while renal plasma flow (RPF) was lower in NP. After CS, both GFR and RPF significantly decreased in the two groups, but the percent decrease in inulin clearance was greater in NP. Filtration fraction increased only in NC. Basal renal vascular resistances were greater in NP, and significantly increased after CS in both groups. Basal fractional sodium excretion (FE(Na)) was lower in NP: after CS FE(Na) decreased only in NC. Neither plasma renin activity, nor plasma aldosterone changed after CS. When urinary protein excretion (U(P)) was corrected by GFR, no change was observed after CS; by contrast, selectivity of proteinuria (as assessed by the C(IgG)/C(Transferrin) ratio) markedly increased. Our data indicate that CS induces a greater fall in the GFR in hypovolemic NP than in healthy subjects, probably because in the former GFR becomes extremely plasma flow dependent. No change in U(P) per unit of GFR is observed after CS, while a striking improvement in urinary protein selectivity occurs, probably as a result of a fall in glomerular ultrafiltration coefficient by CS.

Original languageEnglish
Pages (from-to)369-374
Number of pages6
JournalNephron
Volume59
Issue number3
Publication statusPublished - 1991

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Nephrotic Syndrome
Cyclosporine
Hemodynamics
Kidney
Glomerular Filtration Rate
Proteins
Renal Plasma Flow
Body Weight
Proteinuria
Healthy Volunteers
Hypovolemia
Inulin
Diuresis
Ultrafiltration
Transferrin
Blood Volume
Aldosterone
Renin
Vascular Resistance
Oral Administration

Keywords

  • acute nephrotoxicity
  • ciclosporin
  • nephrotic syndrome

ASJC Scopus subject areas

  • Nephrology

Cite this

Acute effects of ciclosporin on renal hemodynamics and urinary protein excretion in patients with the nephrotic syndrome. / Fuiano, G.; Conte, G.; Sepe, V.; Balletta, M.; Cianfrone, P.; Libetta, C.; Romano, G.; Sabbatini, M.; Bisesti, V.

In: Nephron, Vol. 59, No. 3, 1991, p. 369-374.

Research output: Contribution to journalArticle

Fuiano, G, Conte, G, Sepe, V, Balletta, M, Cianfrone, P, Libetta, C, Romano, G, Sabbatini, M & Bisesti, V 1991, 'Acute effects of ciclosporin on renal hemodynamics and urinary protein excretion in patients with the nephrotic syndrome', Nephron, vol. 59, no. 3, pp. 369-374.
Fuiano, G. ; Conte, G. ; Sepe, V. ; Balletta, M. ; Cianfrone, P. ; Libetta, C. ; Romano, G. ; Sabbatini, M. ; Bisesti, V. / Acute effects of ciclosporin on renal hemodynamics and urinary protein excretion in patients with the nephrotic syndrome. In: Nephron. 1991 ; Vol. 59, No. 3. pp. 369-374.
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AB - The possibility that the renal hemodynamic abnormalities associated with ciclosporin (CS) administration are enhanced in nephrotic patients (NP), leading to severe impairment of renal function and/or to modifications in proteinuria, has not hitherto been tested. Ten NP and 8 healthy subjects (NC) were examined before and after oral CS administration (10 mg/kg body weight in NP and 12 mg/kg body weight in NC: a lower dosage was adopted in NP because of edema overestimating the actual body weight) under water diuresis by standard renal clearance methods. Basal blood volume was lower in NP. Blood CS levels were not significantly different in the two groups. Basal glomerular filtration rate (GFR) was similar in NP and NC, while renal plasma flow (RPF) was lower in NP. After CS, both GFR and RPF significantly decreased in the two groups, but the percent decrease in inulin clearance was greater in NP. Filtration fraction increased only in NC. Basal renal vascular resistances were greater in NP, and significantly increased after CS in both groups. Basal fractional sodium excretion (FE(Na)) was lower in NP: after CS FE(Na) decreased only in NC. Neither plasma renin activity, nor plasma aldosterone changed after CS. When urinary protein excretion (U(P)) was corrected by GFR, no change was observed after CS; by contrast, selectivity of proteinuria (as assessed by the C(IgG)/C(Transferrin) ratio) markedly increased. Our data indicate that CS induces a greater fall in the GFR in hypovolemic NP than in healthy subjects, probably because in the former GFR becomes extremely plasma flow dependent. No change in U(P) per unit of GFR is observed after CS, while a striking improvement in urinary protein selectivity occurs, probably as a result of a fall in glomerular ultrafiltration coefficient by CS.

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