The precision of estimating protein intake of patients with chronic renal failure

Masud, Tahsin; Manatunga, Amita K.; Cotsonis, George

doi:10.1046/j.1523-1755.2002.00606.x

Cited by 71 publications

(41 citation statements)

References 27 publications

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“…The use of this formula will be called a strength by some because of the objective way of measuring protein intake and a limitation by others because of the lack of detailed information about food intake (e.g., kind of protein and amount of energy intake). It has been proved, however, that this formula is a valid method to estimate actual protein intake, 22 whereas it is also known that questionnaire-based methods are associated with both random and systematic error. 14,15 Moreover, the average amount of protein we found in our population is comparable with the values reported in another study using the Maroni formula to estimate the amount of protein intake in a Japanese community-based cohort.…”

Section: Discussionmentioning

confidence: 99%

High Protein Intake Associates with Cardiovascular Events but not with Loss of Renal Function

Halbesma¹,

Bakker²,

Jansen³

et al. 2009

Journal of the American Society of Nephrology

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The long-term effects of higher dietary protein intake on cardiovascular and renal outcomes in the general population are not clear. We analyzed data from 8461 individuals who did not have renal disease and participated in two or three subsequent screenings (6.4-yr follow-up) in a prospective, communitybased cohort study (Prevention of Renal and Vascular ENd-stage Disease [PREVEND]). We calculated daily protein intake from 24-h urinary urea excretion (Maroni formula) and used Cox proportional hazard models to analyze the associations between protein intake, cardiovascular events, and mortality. We used mixed-effects models to investigate the association between protein intake and change in renal function over time. The mean Ϯ SD daily protein intake was 1.20 Ϯ 0.27 g/kg. Protein intake was significantly associated with cardiovascular events during follow-up. The associations seemed U-shaped; compared with intermediate protein intake, individuals with either higher or lower protein intake had higher event rates. All-cause mortality and noncardiovascular mortality also were significantly associated with protein intake; individuals with low protein intake had the highest event rates. We found no association between baseline protein intake and rate of renal function decline during follow-up. In summary, in the general population, high protein intake does not promote accelerated decline of renal function but does associate with an increased risk for cardiovascular events.

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Section: Discussionmentioning

confidence: 99%

High Protein Intake Associates with Cardiovascular Events but not with Loss of Renal Function

Halbesma¹,

Bakker²,

Jansen³

et al. 2009

Journal of the American Society of Nephrology

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“…Second, the nonurea nitrogen in grams of nitrogen excreted per day is calculated as the excretion of all forms of nitrogen except urea. This amount is approximated as 0.031 g nitrogen/kg per day multiplied by the nonedematous, ideal body weight (4,89). Third, the nonurea nitrogen is subtracted from the nitrogen intake to obtain the amount of urea nitrogen that must be excreted each day in the steady state.…”

Section: Clinical Usesmentioning

confidence: 99%

“…The only other assumption is that urea clearance is independent of the plasma urea concentration, which is reasonable for patients with CKD. The key concept is that steady-state concentrations of nitrogen-containing waste product produced during protein catabolism will increase in parallel to an increase in the S SUN (4,82,89). By varying the amount of dietary protein, changes in the diet can be integrated with different values of the S SUN.…”

Section: Clinical Usesmentioning

confidence: 99%

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Urea and Ammonia Metabolism and the Control of Renal Nitrogen Excretion

Weiner

Mitch

Sands

2015

Clinical Journal of the American Society of Nephrology

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370

265

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Renal nitrogen metabolism primarily involves urea and ammonia metabolism, and is essential to normal health. Urea is the largest circulating pool of nitrogen, excluding nitrogen in circulating proteins, and its production changes in parallel to the degradation of dietary and endogenous proteins. In addition to serving as a way to excrete nitrogen, urea transport, mediated through specific urea transport proteins, mediates a central role in the urine concentrating mechanism. Renal ammonia excretion, although often considered only in the context of acidbase homeostasis, accounts for approximately 10% of total renal nitrogen excretion under basal conditions, but can increase substantially in a variety of clinical conditions. Because renal ammonia metabolism requires intrarenal ammoniagenesis from glutamine, changes in factors regulating renal ammonia metabolism can have important effects on glutamine in addition to nitrogen balance. This review covers aspects of protein metabolism and the control of the two major molecules involved in renal nitrogen excretion: urea and ammonia. Both urea and ammonia transport can be altered by glucocorticoids and hypokalemia, two conditions that also affect protein metabolism. Clinical conditions associated with altered urine concentrating ability or water homeostasis can result in changes in urea excretion and urea transporters. Clinical conditions associated with altered ammonia excretion can have important effects on nitrogen balance.

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“…Dietary data were converted into daily nutrient intake using the Dutch Food Composition Table of 2006 (15). The validity of the FFQ in RTRs was checked by comparing the estimated protein intake with calculations of protein intake according to the Maroni formula, based on 24-hour urinary urea excretion, reliably reflecting protein intake (16,17 Second, we estimated dietary acid load using the algorithm described by Frassetto et al (9):…”

Section: Assessment Of Diet and Acid Loadmentioning

confidence: 99%

Dietary Acid Load and Metabolic Acidosis in Renal Transplant Recipients

Berg

Engberink

Brink

et al. 2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Acidosis is prevalent among renal transplant recipients (RTRs) and adversely affects cardiometabolic processes. Factors contributing to acidosis are graft dysfunction and immunosuppressive drugs. Little is known about the potential influence of diet on acidosis in RTRs. This study examined the association of metabolic acid load with acidosis and with cardiovascular risk factors in RTRs and aimed to identify dietary factors associated with acidosis.Design, participants, setting, & measurements 707 RTRs were included. Metabolic acid load was assessed by measuring 24-hour urinary net acid excretion (NAE; i.e., titratable acid + ammonium 2 bicarbonate). Acidosis was defined as serum [HCO 3 2 ] , 24 mmol/L. BP and insulin resistance, reflected by hemoglobin A1c, were among cardiovascular risk factors. Diet was assessed with food-frequency questionnaires. Linear regression analysis was applied to investigate association between NAE and acidosis and between dietary factors and acidosis.Results Mean age 6 SD was 53613 years; 57% of patients were male. Acidosis was present in 31% of RTRs. NAE was associated with acidosis (serum HCO 3 2 : b=20.61; serum pH: b=20.010; both P,0.001). Patients with high intake of animal protein (i.e., from meat, cheese, and fish) and low intake of fruits and vegetables had significantly lower serum HCO 3 2 and serum pH. No associations were observed between NAE and cardiovascular risk factors, such as hypertension and insulin resistance.Conclusions In addition to conventional factors contributing to acidosis, diet might influence acid-base homeostasis in RTRs. Higher intake of fruits and vegetables and lower animal protein intake is associated with less acidosis in RTRs.

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The precision of estimating protein intake of patients with chronic renal failure

Abstract: Fecal nitrogen is not correlated with IN. NUN is not constant but varies with weight, and the traditional method of estimating IN in stable chronic renal insufficiency (CRI) patients from UNA and weight as proposed by Maroni, Steinman, and Mitch is valid.

Cited by 71 publications

References 27 publications

High Protein Intake Associates with Cardiovascular Events but not with Loss of Renal Function

High Protein Intake Associates with Cardiovascular Events but not with Loss of Renal Function

Urea and Ammonia Metabolism and the Control of Renal Nitrogen Excretion

Dietary Acid Load and Metabolic Acidosis in Renal Transplant Recipients

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