Short-Term Effect of Low and High Protein Intake on Renal Function in Children with Renal Disease

Excess protein and amino acid intake have been recognized as hazardous potential implications for kidney function, leading to progressive impairment of this organ. It has been suggested in the literature, without clear evidence, that high protein intake by athletes has no harmful consequences on renal function. This study investigated body-builders (BB) and other well-trained athletes (OA) with high and medium protein intake, respectively, in order to shed light on this issue. The athletes underwent a 7-day nutrition record analysis as well as blood sample and urine collection to determine the potential renal consequences of a high protein intake. The data revealed that despite higher plasma concentration of uric acid and calcium. Group BB had renal clearances of creatinine, urea, and albumin that were within the normal range. The nitrogen balance for both groups became positive when daily protein intake exceeded 1.26 g · kg−1 but there were no correlations between protein intake and creatinine clearance, albumin excretion rate, and calcium excretion rate. To conclude, it appears that protein intake under 2.8 g·kg−1 does not impair renal function in well-trained athletes as indicated by the measures of renal function used in this study.

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Renal effects of prolonged high protein intake and COX2 inhibition on hypertensive rats with altered renal development

AJP Renal Physiology ◽

10.1152/ajprenal.00110.2011 ◽

2011 ◽

Vol 301 (2) ◽

pp. F327-F333 ◽

Cited By ~ 9

Author(s):

Virginia Reverte ◽

Antonio Tapia ◽

Juan Manuel Moreno ◽

Leocadio Rodríguez ◽

Francisco Salazar ◽

...

Keyword(s):

Renal Function ◽

Protein Intake ◽

High Protein ◽

Renal Development ◽

Sprague Dawley ◽

Hypertensive Rats ◽

High Protein Intake ◽

Renal Vasoconstriction ◽

Renal Ablation

Cyclooxygenase 2 (COX2) is involved in regulating renal hemodynamics after renal ablation. It is also known that high protein intake (HPI) leads to a deterioration of renal function when there is preexisting renal disease and that there are important gender differences in the regulation of renal function. This study tested the hypothesis that the role of COX2 in regulating renal function and the renal hemodynamic effects elicited by HPI are enhanced when nephrogenesis is altered during renal development. It was also expected that the role of COX2 and the effects elicited by HPI are age and sex dependent. Newborn Sprague-Dawley rats were treated with an AT1 ANG II receptor antagonist during the nephrogenic period (ARAnp). Experiments were performed at 3–4 and 10–11 mo of age. Arterial pressure was elevated ( P < 0.05) at both ages and in both sexes of ARAnp-treated rats. Renal COX2 expression was only elevated ( P < 0.05) at 10–11 mo of age in both sexes of ARAnp-treated rats. COX2 inhibition induced greater renal vasoconstriction in male and female hypertensive than in normotensive rats at both ages. HPI did not induce glomerular filtration rate (GFR) in the youngest hypertensive rats and in the oldest female hypertensive rats. However, the GFR decreased during HPI (0.63 ± 0.07 to 0.19 ± 0.05 ml/min) in the oldest male hypertensive rats. The HPI-induced increment in proteinuria was greater ( P < 0.05) in male (99 ± 22 mg/day) than in female (30 ± 8 mg/day) hypertensive rats. These results show that COX2 plays an important role in the regulation of renal function when renal development is altered and that prolonged HPI can lead to a renal insufficiency in males but not in females with reduced nephron endowment.

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