Irrespective of the underlying renal disease, the loss of renal functi
on progresses continuously over time in most forms of chronic renal di
seases. This process involves glomerular hemodynamic and nonhemodynami
c factors, which, through glomerular hyperperfusion, hyperfiltration a
s well as hypertension and through hypertrophy (enlargement) cause glo
merulosclerosis, tubulo-interstitial fibrosis and vascular sclerosis.
The improved understanding of the pathophysiology of CRF suggests new
therapeutic approaches. Large, representative studies conducted over t
he past few years have shown that the progression of chronic renal ins
ufficiency can be slowed or even stopped by antihypertensive agents (A
CE inhibitors), and dietary protein restriction. Normalizing the serum
liquid profile, high diuresis, controlling acidosis, and cessation of
smoking may also be effective in this respect. In animal experiments,
protein restriction influences the functional and morphological distu
rbances of the adaptation process through alteration of growth factors
(TGF beta, PDGF) and endocrine systems like glucagon, renin, and othe
rs and may have a renoprotective effect. The influence of a low-protei
n diet on the progression of chronic renal insufficiency in humans has
been investigated in studies relating to diabetic and nondiabetic ren
al diseases, through the results being partly conflicting. In all, met
aanalyses by Fouque and Pedrini have confirmed the positive effect of
protein restriction in chronic renal insufficiency. The Modification o
f Diet in Renal Disease (MDRD) Study has shown that protein restrictio
n to 0.6 g/kg/day for patients in an advanced stage of renal insuffici
ency (creatinine clearance 13-24 ml/min) will slow its progression. In
contrast, a further reduction of protein supply combined with a suppl
ementation of essential aminoacids and ketoacids did not yield any fav
orable results. Taken together, these studies and a consensus conferen
ce held in 1994 recommend that patients with a moderate impairment of
renal function (GFR 25-55 ml/min) should be restricted to 0/6 g/kg/day
. In this case, the nutritional status should be checked by determinin
g body weight, serum albumin, and transferrin levels. Energy supply mu
st be increased to 30-35 kcal/kg/day, if necessary. Target blood press
ure for patients with renal insufficiency and proteinuria > 1 g/day sh
ould be 125/75 mmHg (the mean arterial blood pressure being 92 mmHg).
ACE inhibitors play a leading role in antihypertensive therapy. Accord
ing to Gansevoort, the combination of ACE blocker and protein restrict
ion may cause a significantly sharper decline of proteinuria than the
2 individual components alone. Moreover, a protein-restrictive diet al
so helps to reduce phosphate and lipid supply, thus obtaining probably
additional protective effects on chronic renal failure.