In 6 volunteers with normal renal function, we investigated the effects of various kinds of protein (soy, lactoprotein and beef) and various amounts of an intravenously administered amino acid solution on glomerular filtration (GFR) and effective renal plasma flow (ERPF). As for the protein-induced changes in renal function, rises in GFR and ERPF were lowest with soy protein, and highest with beef (baseline GFR, 110 ± 5; soy, 122 ± 5; beef, 131 ± 5 ml/min/1.73 m²; mean ± SEM). High doses of intravenous amino acids induced arise in GFR comparable to that after beef (132 ± 5 ml/min/1.73 m²). In a combined test a liquid mixed meal together with intravenously administered amino acids induced a comparable increase of the GFR (baseline 114 ± 5 versus 129 ± 5 ml/min/1.73 m²). When investigating 9 patients with chronic renal insufficiency after 4 weeks of low protein intake (LP) and after 4 weeks of high protein intake (HP), GFR and ERPF rose significantly under baseline conditions (GFR-LP 41 ± 9 versus GFR-HP 45 ± 9 ml/min/1.73 m², p < 0.02; ERPF-LP 169 ± 39 versus ERPF-HP 180 ± 40 ml/min/1.73 m², p < 0.02; paired Wilcoxon). At the end of both dietary periods a comparable rise in renal function could be induced through acute stimulation (GFR-LP 20 ± 5, GFR-HP 16 ± 4; ERPF-LP 23 ± 7, ERPF-HP 22 ± 3%). Glucagon levels tended to fall during a HP diet (glucagon-LP 69 ± 11 versus glucagon HP 50 ± 12 ng/l), whereas an acute rise in glucagon levels could be induced by acute stimulation at the end of both dietary periods (glucagon-LP 163 ± 18, glucagon-HP 173 ± 58%). We conclude that renal function remains variable even in patients with moderate to severe renal insufficiency and that acute stimulation remains possible to the same extent after LP and HP intake. Our results also suggest different underlying mechanisms for the acute and chronic stimulation of renal function.

In 30 patients with chronic renal disease, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured after 4 weeks of protein restriction and subsequently after adhering to a high protein intake for the same period. Twenty-four patients adhered to their advised diets according to the 24-hour urea excretion. These 24 patients showed a significant increase in GFR, ERPF and proteinuria (n = 15) during a high protein intake, even if their renal function was markedly impaired. It is concluded that although in patients with markedly impaired renal function a meat meal or an infusion of amino acids does not change renal function anymore, prolonged high protein intake is accompanied by an increase in GFR, poorly dependent on GFR after prolonged protein restriction.

No abstract

Protein restriction is advocated in patients with chronic renal insufficiency (CRI) in an attempt to slow down further renal function deterioration, with the most obvious effect in patients with chronic glomerulonephritis (GN) and diabetic nephropathy, and much less in other disease entities, such as adult polycystic kidney disease (APKD), tubulointerstitial nephritis (TIN) and nephrosclerosis (NS). The mechanism by which protein restriction slows down the progression of renal failure remains unclear. Decline of hyperfiltration has been implicated. Whether long-term protein restriction in patients with CRI is associated with a decrease in hyperfiltration is not clear. We studied the effects of prolonged protein intake variation (isocaloric diets in 4-week periods of low (goal: 30-40 g protein daily) and high protein intake (goal: 80-90 g daily) on renal function in 51 patients with CRI. Patients were divided into subgroups according to the underlying renal disease (GN, n = 17; APKD, n = 9; TIN, n = 12; NS, n = 13). Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured at the end of each study period. Overall, GFR rose from 39 (9-90) to 46 (9-100) ml/min/1.73 m² (median and ranges, p < 0.01), and ERPF from 158 (39-558) to 171 (32-676) ml/min/1.73 m² (p < 0.01). GFR rose significantly in GN (15%, range -23 to 51%), APKD (5%, range -10 to 33%), and NS (8%, range -8 to 25%). ERPF only rose significantly in GN (14%, range -45 to 47%) and APKD (9%, range -9 to 25%). It can be speculated that an inability to vary ERPF with dietary changes would implicate a decreased or lost renal vascular reactivity. Thus, it could be that the beneficial effects of protein restriction in CRI can be expected only in those patients in whom renal blood flow varies when changing protein intake, i.e., in patients with GN and, to a lesser extent, in patients with APKD.