Effects of an Oral Protein Load on Glomerular Filtration Rate in Healthy Controls and Nephrotic Patients

Mizuiri, Sonoo; Hayashi, Ikuko; Ozawa, Takashi; Hirata, Kiyofumi; Takano, Masaaki; Sasaki, Yasuhito

doi:10.1159/000184886

Cited by 17 publications

(7 citation statements)

References 18 publications

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“…The results of this study support the previous findings that an acute increase in protein intake can stimulate GFR also in patients with diseased kidneys [6,7,9]; moreover, they demonstrate that the hemodynamic changes following a protein load may affect the renal handling of sodium and water. Both these hemodynamic and physiologic changes are apparently blunted by pre treatment with the ACE inhibitor enalapril.…”

Section: Discussionsupporting

confidence: 90%

Effects of a Protein Load in Patients with Early Chronic Renal Failure before and after Angiotensin II Blockade

Oldrizzi

Rugiu²,

Maschio³

1989

Nephron

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We studied the effects of mid-term enalapril administration on protein-load-induced renal responses in 10 patients with early chronic renal failure (serum creatinine 2.70 ± 1.0 mg/dl). The oral protein load was performed twice, before and after a 10-day therapy with enalapril. Glomerular filtration rate (¹²⁵I-iothalamate clearance) rose from 22.5 ± 10.6 to 60.1 ± 32.8 ml/min after the protein load before enalapril; it did not change after the protein load during enalapril therapy. Percent fractional excretion of sodium, urinary osmolality and free water clearance were significantly affected only by the protein load before enalapril. Enalapril blunts the protein-load-induced changes in glomerular filtration rate and in tubular function; these effects might be mediated by angiotensin II blockade.

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Section: Discussionsupporting

confidence: 90%

Effects of a Protein Load in Patients with Early Chronic Renal Failure before and after Angiotensin II Blockade

Oldrizzi

Rugiu²,

Maschio³

1989

Nephron

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“…Reserve capacity of kidneys was lower at patients with HTN-n in comparison with HTN that is probably caused not only with systemic hypertension, but also with presence of glomerular injury, proteinuria, and other factors. 28 Results of our research do not differ from data of Mizuiri S. et al 23 where 50 g of protein intake increased GFR for 15% at healthy subjects, and it varied from 0 to 19.4% at nephropathic patients. Age and duration of hypertension are one of the important factors of renal function decline.…”

Section: Discussionsupporting

confidence: 46%

“…21 Many studies demonstrated response of basal GFR to different stimuli from usual chicken and beef meat intake to amino acid and some drugs infusions in healthy individuals. 8,9,[22][23][24][25][26] In our study we first used …”

Section: Discussionmentioning

confidence: 99%

Renal functional reserve and renal hemodynamics in hypertensive patients

et al. 2016

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The renal functional reserve (RFR) is the ability of the kidneys to increase renal plasma flow and glomerular filtration rate (GFR) in response to protein intake. It is a measure of functional and anatomic integrity of nephrons. It is not known what relation between RFR and kidney Doppler parameters. We aimed to study the relation between the RFR and renal hemodynamic parameters in hypertensive patients with and without nephropathy who had normal kidney function. Twenty-four hypertensive subjects with nephropathy (HTN-n, n ¼ 10) and hypertension without nephropathy (HTN, n ¼ 14) were included in the study. Control group included 11 healthy subjects. Baseline GFR (GFR1) and GFR after intake of egg protein 1 mg/kg of body weight were determined (GFR2). RFR was calculated by the following formula: (GFR2-GFR1)/GFR1 Â 100%. Doppler ultrasonography was performed. Arterial blood pressure (BP), body mass index (BMI), and estimated GFR were also recorded. HTN and HTN-n groups had impaired levels of RFR compared with controls (p < 0.05), significantly decreased value of flow velocity parameters (Vmax, Vmin), and increased RRI compared with controls. There was significant negative correlation of RFR with blood pressure levels (sBP, r ¼ À0.435, p ¼ 0.009; dBP, r ¼ À0.504, p ¼ 0.002), RRI (r ¼ À0.456, p ¼ 0.008), micro albuminuria (MAU, r ¼ À0.366, p ¼ 0.031) and positive correlation with Vmax and Vmin (r ¼ 0.556, p ¼ 0.001 and r ¼ 0.643, respectively, p < 0.001). Linear regression showed that RRI and MAU were independent predictors of decreased RFR. RFR is lower in hypertensive patients despite near-normal level of kidney function and is related to particular level of BP. RRI and MAU were independent predictors of decreased RFR. ARTICLE HISTORY

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“…Renal functional reserve is thought to be reduced or lost entirely when renal mass falls below a certain limit [7,8]. A lowered renal functional reserve has been reported in patients with nephrotic syndrome [9], IgA-nephritis [7] in patients after nephrectomy [3] and after renal transplanta tion [10,11].…”

Section: Discussionmentioning

confidence: 99%

Influence of the Renin-Angiotensin System and Atrial Natriuretic Peptide on Renal Functional Reserve

Heering

Wyes²,

Plum³

et al. 1994

Nephron

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We studied the renin-angiotensin system (RAS) and atrial natriuretic peptide (ANP) after amino acid loading in order to elucidate whether or not glomerular hyperfiltration is mediated by these hormones. Eight healthy controls without kidney disease (grop 1), 8 renal graft recipients (group 2) and 8 patients after nephrectomy (group 3) werde studied. Furthermore, we investigated the influence of amino acid loading on RAS and ANP and glomerular filtration during acute application of captopril in healthy controls. Clearances in inulin (C_In) and para-aminohippuric acid (C_PAH) werde determined during an infusion of 0.9% saline and during amino acid loading. C_In increased in healthy controls from 96.5 ± 3.3 to 111.9 ± 4.4 ml/min (p < 0.01), C_PAH rose from 577 ± 28.7 to 618.9 ± 38 ml/min (p = NS). During the combined application of amino acid infusion and 25 mg captopril, C_IN increased to 125.0 ± 16.4 ml/min/1.73 m² (p < 0.01) and there was no significant increase in C_PAH which was 595 ± 77 ml/min/1.73 m². There was no significant change in renal vascular resistance, but filtration fraction increased from 17 ± 1 to 19 ± 1% under amino acid infusion and increased further under the application of captopril to 21 ± 2% (p < 0.05). In renal graft recipients, C_In had a tendency to increase during amino acid infusion from 78.4 ± 5.8 to 84.7 ± 6.5 ml/min (p = NS). In patients after nephrectomy, C_In did not increase (84.5 ± 6 ml/min) but C_PAH did from 345.7 ± 26.3 to 409 ± 24.1 ml/min (p < 0.05). In healthy controls, ANP was not increased during amino acid infusion: 80.5 ± 9.3 pg/ml as compared to saline infusion with 62.0 ± 10.6 pg/ml (p = NS). During the administration of amino acid infusion in renal graft recipients, ANP was not increased: 283 ± 62.7 as compared to 334 ± 115.7 pg/ml under saline infusion. A renal functional reserve could be shown in healthy persons, but this was grossly diminished in graft recipients and patients after unilateral nephrectomy. Renal functional reserve was maintained in healthy controls during the application of captopril. This investigation indicates that the increase in glomerular filtration rate seen in healthy persons is not mediated by RAS or ANP.

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Effects of an Oral Protein Load on Glomerular Filtration Rate in Healthy Controls and Nephrotic Patients

Cited by 17 publications

References 18 publications

Effects of a Protein Load in Patients with Early Chronic Renal Failure before and after Angiotensin II Blockade

Effects of a Protein Load in Patients with Early Chronic Renal Failure before and after Angiotensin II Blockade

Renal functional reserve and renal hemodynamics in hypertensive patients

Influence of the Renin-Angiotensin System and Atrial Natriuretic Peptide on Renal Functional Reserve

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