Ljm. Reichert et al., Acute haemodynamic and proteinuric effects of prednisolone in patients with a nephrotic syndrome, NEPH DIAL T, 14(1), 1999, pp. 91-97
Background. Administration of prednisolone causes an abrupt rise in protein
uria in patients with a nephrotic syndrome.
Methods. To clarify the mechanisms responsible for this increase in protein
uria we have performed a placebo controlled study in 26 patients with a nep
hrotic syndrome. Systemic and renal haemodynamics and urinary protein excre
tion were measured after prednisolone and after placebo.
Results. After i.v. administration of 125-150mg prednisolone total proteinu
ria increased from 6.66 +/- 4.42 to 9.37 +/- 6.07 mg/min (P < 0.001). By an
alysing the excretion of proteins with different charge and weight (albumin
, transferrin, IgG, IgG(4) and beta(2)-microglobulin) it became apparent th
at the increase of proteinuria was the result of a change in size selectivi
ty rather than a change in glomerular charge selectivity or tubular protein
reabsorption. Glomerular filtration rate rose from 83 +/- 34 ml to 95 +/-
43 ml/min (P < 0.001) after 5 h, whereas effective renal plasma flow and en
dogenous creatinine clearance remained unchanged. As a result filtration fr
action was increased, compatible with an increased glomerular pressure, whi
ch probably contributes to the size selectivity changes. Since cortico-ster
oids affect both the renin-angiotensin system and renal prostaglandins, we
have evaluated the effects of prednisolone on proteinuria after pretreatmen
t with 3 months of the angiotensin-converting enzyme inhibitor lisinopril o
r after 2 weeks of the prostaglandin synthesis inhibitor indomethacin. Neit
her drug had any effect on prednisolone-induced increases of proteinuria.
Conclusions. Prednisolone increases proteinuria by changing the size select
ive barrier of the glomerular capillary. Neither the renin-angiotensin axis
nor prostaglandins seem to be involved in these effects of prednisolone on
proteinuria.