The effect of different intravenous nutritional regimens on renal regeneration during acute renal failure in the rat

Acute renal failure in the surgical patient is accompanied by a state of hypermetabolism and increased catabolism. Nutritional therapy is therefore directed at the preservation of body cell mass and protein synthesis for repair of wounds, repair of the damaged renal tubuli and maintenance of host defense mechanisms. We examined the effect of two levels of protein intake (18.4 ± 1.4 and 30.8 ± 2.4 mg N/100 g BW/day) and three different amino-acid formulations (Freamine III^®, Nephramine^® and a made-up mixture of Nephramine^® ± Freamine^® HBC) on renal regeneration following mercury chloride-induced acute renal failure in the rat. All animals suffered severe renal failure manifested by increased plasma urea and creatinine levels, decreased creatinine clearance and increased fractional excretion of sodium. Incorporation of ³H-thymidine into renal DNA on day 4 of acute renal failure was similar in all six groups studied, irrespective of the amount or composition of amino-acids infused. Renal regeneration during acute renal failure in the rat seems not to be affected either by the quantity or quality of amino-acids infused. However, although not reaching statistical significance, increased amounts of a standard TPN formulation may depress renal regeneration.     

Total parenteral nutrition in the management of acute renal failure.

Malnutrition is frequently present in patients with acute renal failure and may affect morbidity and mortality in this condition. When adequate nourishment cannot be given through the gastrointestinal tract, total parental nutrition with amino acids and hypertonic glucose may have beneficial results. Total parenteral nutrition has been reported to stabilize or reduce serum urea nitrogen, potassium and phosphorus levels, improve wound healing, enhance survival from acute renal failure, and possibly increase the rate of recovery of renal function. The optimal composition of the total parenteral nutrition infusate is unknown. Preliminary results of a double-blind study are reported in which one man received hypertonic glucose alone, two received glucose with essential amino acids (21 g/day), and three received glucose with essential (21 g/day) and nonessential (21 g/day) amino acids. All infusates were isocaloric. No differences were observed in serum urea nitrogen levels, serum urea nitrogen/creatinine ratios or urea appearance rates. Nitrogen balance was negative in all patients. The ratio of essential amino acids/nonessential amino acids were higher and the tyrosine/phenylalanine ratios were lower in plasma in the two patients receiving glucose with essential amino acids. No patient survived the hospitalization. In view of the markedly negative nitrogen balance frequently observed in these and earlier studies, the use of a different composition or quantity of amino acids, a higher energy intake, and anabolic hormones deserve further investigation.     

Low protein diet and ketosteril in predialysis patients with renal failure

After a short review of the contemporary understanding of amino acid supplementation to low protein diets in patients with uremia we present the results of administration of ketosteril in 20 low-protein-diet patients on such a diet. MATERIAL AND METHODS: Twenty patients (10 men and 10 women) with stable II and III stage chronic renal failure were assigned to a low protein diet (protein up to 40 g/day). Ketosteril (6 tablets a day) were added to the diet. Some of the basic markers of protein metabolism and nitrogen balance were followed. RESULTS: No evidence of deteriorated protein synthesis was found in the therapy thus administered. Serum urea and creatinine values did not change and even tended to decrease. Glomerular filtration was found to increase insignificantly more markedly in the patients with renal failure in the early stages. CONCLUSIONS: A low protein diet with increased content of essential amino acids and their keto-analogues does not deteriorate the nitrogen balance of patients with chronic renal failure. By adding essential amino acids and keto-analogues a normal protein metabolism is maintained in spite of the reduce intake of protein substances with the diet. Supplementation of the diet of chronic renal failure patients with essential amino acids and keto-analogues allows a considerable reduction of the protein intake to be achieved which brings about reduction of glomerular hyperfiltration which actually retards the progression of renal failure and improves its short-term prognosis.     

Effects of catabolic stress in acute and chronic renal failure

The degree of catabolism was studied in a group of seven patients with postsurgical acute renal failure, and net protein catabolism of 43.1 to 927 g/day. In 70% of a group of 30 patients with stable chronic renal failure receiving and 18 g high biological value protein diet, urea synthesis was equivalent to what could be accounted for by the protein content of the food. This equivalence was not found in studies in both adults and children who were treated for catabolic chronic renal failure. Data obtained show the superiority of feeding essential amino acids with an adequated caloric supply. The need for studies aimed at adapting the uremic patient to protein depletive mechanisms is strongly stressed.     

Resting metabolic rate in chronic renal failure.

OBJECTIVE: A decrease in resting metabolic rate (RMR) in patients with chronic renal failure was assumed to occur because of the decreasing oxygen consumption of the kidneys, which in healthy subjects, accounts for 7.2% of RMR. Contrary to this assumption, RMR per body weight in end-stage renal disease was increased. DESIGN AND METHODS: To test the impact of chronic renal failure on the RMR, direct bedside calorimetry was performed on 51 outpatients (age, 53.2 +/- 13.9 y; creatinine clearance, 6.9 to 52 mL/min). Twenty two of 51 patients were examined repeatedly (at the start of the study, after 3 months, and after 6 months) during declining kidney function. RESULTS: In the total group, RMR per body weight (RMR/BW) was 100.0 +/- 4.96 kJ/kg/day and RMR per body surface area (RMR/BSA) was 4.582 +/- 0.181 kJ/min/1.73m(2). RMR/BW and RMR/BSA correlated significantly with creatinine clearance (n = 51, r = -.763, P <.001; n = 51, r = -.557, P <.001). In the follow-up group, creatinine clearance decreased from 27.5 +/- 9.5 mL/min initially, to 19.4 +/- 6.25 mL/min at 3 months, to 13.0 +/- 3.8 mL/min at 6 months (P <.001), while RMR/BW and RMR/BSA increased from 98.28 +/- 6.3, to 101.64 +/- 5.46, to 105.42 +/- 6.3 kJ/kg BW/d (P <.005), respectively, and 4.41 +/- 0.126, to 4.578 +/- 0.168, to 4.704 +/- 0.168 kJ/min/1.73 m(2) (P <.05), respectively. CONCLUSION: Taking into account the reduced oxygen consumption of the shrinking kidneys, the normal RMR suggests an increased energy expenditure per body cell mass. The raising RMR in deteriorating excretory kidney function reflects the increasing energy expenditure in progressive chronic renal failure.     

Growth of rats with severe renal insufficiency fed a formula designed to minimize urinary solutes

Experiments were designed to test the hypothesis that growth depression and azotemia in chronic renal failure can be minimized by providing a nutritional formula that is adequate is essential nutrients but minimizes urinary excretion of all solutes. Unrestrained rats were fed exclusively by continuous intragastric infusion with a mixture containing sucrose, essential amino acids, N-free analogues thereof, minerals, corn oil, and vitamins, designed to minimize urinary solute excretion while permitting growth. After 5 days, renal excretory function was reduced to 1/10 by reinfusing 90% of each day's urinary output intragastrically for the next 3 wk. Weight gain (3.6 +/- 0.1 g/day), linear growth and carcass N accretion were the same as in nonreinfused rats receiving substantially the same formula by intragastric catheter. Except for sight acidosis (CO2 18.5 mM) accumulation of electrolytes did not occur. Average final serum urea N was only 42.5 +/- 7.1 mg/dl. The results are considered as supporting the hypothesis.     

Effect of cyclosporine on the rate of renal function recovery after renal transplantation

To assess the effect of cyclosporine therapy on the rate of renal function recovery after renal transplantation, patients with no clinical evidence of rejection and who were treated with either cyclosporine or azathioprine in addition to steroid therapy were studied (n = 74). Of the patients with immediate renal function (n = 57), those receiving organs from living, related donors had a faster recovery rate of glomerular filtration than patients with cadaveric grafts (azathioprine, 15 +/- 2 versus 7 +/- 1 mL/min/day, P = 0.0001; cyclosporine, 14 +/- 3 versus 6 +/- 1 mL/min/day, P = 0.001). Recipients of cadaveric grafts with delayed renal function (n = 17) had a decreased recovery rate of allograft function when treated with cyclosporine as compared to those treated with azathioprine (4 +/- 2 versus 6 +/- 1 mL/min/day, respectively; P = 0.026). Patients on azathioprine achieved better renal function (P = 0.01) than those on cyclosporine (recipients of organs from living, related donors, 59 +/- 5 versus 52 +/- 3 mL/min; recipients of cadaveric grafts, 52 +/- 5 versus 40 +/- 2 mL/min). Thus, even in this early period, cadaveric-graft recipients treated with cyclosporine demonstrate an apparent reduction in creatinine clearance when compared to patients treated with azathioprine.     

Influence of a novel amino acid solution (enriched with the dipeptide glycyl-tyrosine) on plasma amino acid concentration of patients with acute renal failure

In this randomized, double-blind controlled study we compared the effect of parenteralnutrition with two different amino acid solutions on the plasma concentration of amino acids in 27 patients with acute renal failure. Fourteen patients received the new dipeptide-containing (glycyl-tyrosine) amino acid solution (AADI) in combination with glucose (60%) and fat (10%) as an 'all-in-one' solution over 120 h continuously via a central venous catheter. In the control group (AAST), parenteral nutrition with a standard amino acid solution in isonitrogenous and isocaloric form (0.7 g amino acids/kg BW/day and 25 kcal/kg BW/day) was administered to 13 patients over the same period of time. The administration of the dipeptide-containing amino acid solution caused a return to within the normal range of most of the amino acid concentrations which were decreased at the onset. A significant difference could be found between the AADI and AAST group for the achieved plasma concentrations of threonine (P < 0.01), phenylalanine (P<0.05), isoleucine (P<0.05), tryptophan (P<0.01) and ornithine (P<0.05), The phenylalanine/tyrosine ratio, did not change in the AADI group, while a marked increase was observed in the AAST group. (152.7 +/- 23.5 - 159.8 +/- 37.6 vs 172.6 +/- 24.6 - 310.6 +/- 136.7, respectively). The plasma concentration of glycyl-tyrosine was at the limit of detectability indicating rapid hydrolysis of the dipeptide in acute renal failure. These data suggest that the new dipeptide-containing amino acid solution offers a clear advantage over a standard amino acid formulation in correcting the amino acid imbalances in plasma of patients with ARF and is able to maintain normal tyrosine concentrations and phenylalanine/tyrosine ratio.     

Full protein alimentation and nitrogen equilibrium in a renal failure patient treated with continuous hemodiafiltration: a case report of 67 days of continuous hemodiafiltration.

Standard care for patients with renal failure while in an intensive care unit involves traditional hemodialysis or peritoneal dialysis and protein restriction. We present a case of a patient with renal failure supported with continuous arteriovenous hemofiltration with dialysis (CAVH-D) who was given full protein alimentation. Total daily urea clearance was measured from the CAVH-D output. Protein load was 196 +/- 34 g/day while receiving total parenteral nutrition and 164 +/- 30 g/day while receiving enteral alimentation. Serum blood urea nitrogen was controlled between 40 and 75 mg/dL, except during septic episodes. Nitrogen balance was estimated based upon known alimentation protein load and measurable and estimated nitrogenous losses. The patient was potentially in nitrogen equilibrium during most of the dialysis period. The cumulative nitrogen balance was positive by 5.2 g after 67 days of dialysis. Volume of alimentation was 3.49 +/- 0.7 liters/day. With CAVH-D, the renal failure patient can receive full alimentation without volume or protein load limitations. Furthermore, nitrogen balances can be estimated easily while the patient is on CAVH-D.     

Recombinant human growth hormone in patients with acute renal failure.

OBJECTIVE: The objective of this study is to determine the impact of recombinant human growth hormone (rhGH) on metabolic and nutritional parameters in malnourished patients with acute renal failure. DESIGN: The design is an open-labeled pilot trial examining the effects of rhGH administration in a small group of highly catabolic, malnourished patients with acute renal failure. Each patient served as his or her own control. SETTING: An intensive care unit in a tertiary care medical institution. PATIENTS: Five patients with established acute renal failure in a critical care unit. Entry criteria included clinical evidence of malnutrition: a serum albumin level of <3.2 g/dL, a prealbumin level of < or = 20 mg/dL, and an insulin-like growth factor IGF 1 level <200 ng/mL. The study consisted of 3 periods: phase I, 3 day baseline; phase II, 6 day treatment; and phase III, 3 day washout. During the entire study, blood and urine samples were obtained daily to calculate normalized protein catabolic rate, total nitrogen appearance rate (TNA), and nitrogen balance. Additional data were collected to measure metabolic and inflammatory parameters. INTERVENTION: The intervention consisted of administering 100 microg/kg/d of rhGH for 6 days. RESULTS: There were significant changes in TNA, normalized protein catabolic rate, and nitrogen balance during the 3 study phases. TNA decreased from 43.3 +/- 24.4 g/d in phase I, to 25.2 +/- 16.5 g/d during phase II (P <.001). There was a further decrease in TNA to 16.2 +/- 8.3 g/d during phase III (P <.001 v phase I). Nitrogen balance improved from - 31.8 +/- 21.4 g/d during phase I, to - 12.9 +/- 10.3 g/d during phase II (P <.001), and further improved to - 4.1 +/- 4.0 g/d in phase III (P <.001 v phase I). Significant changes were also noted in levels of blood urea nitrogen, phosphorous, serum growth hormone, IGF-1, and serum leptin levels after growth hormone administration. A statistically significant increase in serum albumin was noted in phase III (3.1 g/dL) versus phase I (2.7 +/- 0.7 g/dL). CONCLUSIONS: Administration of rhGH to critically ill patients with acute renal failure resulted in improvements in negative nitrogen balance and a significant decrease in total nitrogen appearance rate. These changes corresponded to increases in serum growth hormone, IGF-1, IGF-1 binding protein 3, and leptin levels after growth hormone administration.     

Associations among lead dose biomarkers, uric acid, and renal function in Korean lead workers

Recent research suggests that both uric acid and lead may be nephrotoxic at lower levels than previously recognized. We analyzed data from 803 current and former lead workers to determine whether lead biomarkers were associated with uric acid and whether previously reported associations between lead dose and renal outcomes were altered after adjustment for uric acid. Outcomes included uric acid, blood urea nitrogen, serum creatinine, measured and calculated creatinine clearances, and urinary N-acetyl-ss-d-glucosaminidase (NAG) and retinol-binding protein. Mean (+/- SD) uric acid, tibia lead, and blood lead levels were 4.8 +/- 1.2 mg/dL, 37.2 +/- 40.4 microg/g bone mineral, and 32.0 +/- 15.0 microg/dL, respectively. None of the lead measures (tibia, blood, and dimercaptosuccinic-acid-chelatable lead) was associated with uric acid, after adjustment for age, sex, body mass index, and alcohol use. However, when we examined effect modification by age on these relations, both blood and tibia lead were significantly associated (ss = 0.0111, p < 0.01 and ss = 0.0036, p = 0.04, respectively) in participants in the oldest age tertile. These associations decreased after adjustment for blood pressure and renal function, although blood lead remained significantly associated with uric acid (ss = 0.0156, p = 0.01) when the population was restricted to the oldest tertile of workers with serum creatinine greater than the median (0.86 mg/dL). Next, in models of renal function in all workers, uric acid was significantly (p < 0.05) associated with all renal outcomes except NAG. Finally, in the oldest tertile of workers, associations between lead dose and NAG were unchanged, but fewer associations between the lead biomarkers and the clinical renal outcomes remained significant (p less than or equal to 0.05) after adjustment for uric acid. In conclusion, our data suggest that older workers comprise a susceptible population for increased uric acid due to lead. Uric acid may be one, but not the only, mechanism for lead-related nephrotoxicity.     

Long-term observation of serum creatinine and arterial blood pH in persons with cadmium-induced renal dysfunction

Twenty-one subjects who had cadmium (Cd)-induced renal dysfunction and who lived in a Cd-polluted area in Japan were investigated to determine changes in their renal function. Since 1974, serum creatinine and arterial blood pH were measured annually during the autumn months for 9-14 y. Mean serum creatinine was significantly increased during this period, i.e., from 1.19 +/- 1.28 mg/100 ml to 1.68 +/- 1.56 mg/100 ml. Even after cadmium exposure ceased, significant deterioration of glomerular filtration was found. Eleven subjects showed a greater than 20% serum creatinine increase during this period. The most severe case had a serum creatinine value of 4.4 mg/100 ml at the most recent examination and experienced generalized edema, which suggests a clinical diagnosis of renal failure. The mean arterial blood pH values decreased significantly in all subjects, i.e., from 7.400 +/- 0.023 to 7.361 +/- 0.034. The 11 subjects cited above also showed a significant decrease and progression of tubular dysfunction after Cd exposure ceased. Our findings suggest that Cd-induced renal tubular dysfunction and decreased glomerular filtration are aggravated even after cessation of environmental Cd exposure, and in some cases this renal dysfunction may progress to renal failure.     

Plasma levels of branched chain amino acids in patients on regular hemodialysis before and after including a high-protein supplement in their diet

Chronic renal failure (CRF) patients on hemodialysis have low plasma level of the branched chain amino acids (BCAA) leucine, isoleucine, and valine. The abnormalities in the plasma amino acid pool can be corrected with appropriate high-protein supplements. The present study was designed to evaluate the effect of a balanced protein nutritional supplement on the plasma level of BCAA. Twenty eight CRF patients who received hemodialysis treatment three times in a week were enrolled in the trial. The initial plasma levels of BCAA were as follows--leucine 15.46 +/- 3.88 mcg/ml, isoleucine 9.08 +/- 1.97 mcg/ml, and valine 24.05 +/- 5.06 mcg/ml. For a period of 6 months the patients received a balanced nutritional supplement (58-59% total protein content, leucine--8.6, isoleucine--4.8, and valine--5.7 g/100 g protein) on the day of hemodialysis at a dose 1.0 g/kg body weight. Three months after beginning of supplementation the plasma level of BCAA was found to be elevated--leucine by 36% (P < 0.001), valine by 30% (P < 0.001), and isoleucine by 27% (P < 0.001). The body mass index of the patients was also above the initial values. The plasma BCAA levels were maintained high until the sixth month from the beginning of trial and even a month after withdrawal of the supplement. The results obtained allow us to recommend inclusion of protein supplements with balanced amino acid content in the diet of these patients.     

Protein intake in renal and hepatic disease

The kidney and the liver play a central role in protein metabolism. Synthesis of albumin and other proteins occurs mainly in the liver, whereas protein breakdown and excretion are handled through an intricate interaction between these two organ systems. Thus, disease states of either the liver and/or the kidney invariably result in clinically relevant disturbances of protein metabolism. Conversely, metabolic processes regulated by these two organs are directly affected by dietary protein intake. Of particular importance in this respect is the maintenance of acid/base homeostasis. Finally, both the amount and composition of ingested proteins have a direct impact on renal function, especially in a state of diseased kidneys. Consequently, dietary protein intake is of paramount importance in patients with chronic nephropathy and renal insufficiency. Limitation of ingested protein, particularly from animal sources, is crucial in order to slow the progression of chronic kidney disease and impaired renal function. In contrast, patients with chronic renal failure undergoing renal replacement therapy by hemodialysis or peritoneal dialysis, have an increased protein demand. The syndrome of "protein-energy malnutrition" is a relevant factor for morbidity and mortality in this population and requires early detection and vigorous treatment. Protein intake in patients with cirrhosis of the liver should not be diminished as has been earlier suggested but rather increased to 1.0 - 1.2 g/kg body weight/day, in order to prevent protein malnutrition. Moderate restriction depending on protein tolerance (0.5 - 1.2 g/kg body weight/day), with the possible addition of branched chain amino acids (BCAA), has been recommended only in patients with advanced hepatic encephalopathy. Proteins of plant origin are theoretically superior to animal proteins.     

Impact of increasing parenteral protein loads on amino acid levels and balance in critically ill anuric patients on continuous renal replacement therapy

OBJECTIVES: We wanted to establish optimum protein and glucose intakes during total parenteral nutrition by using a constant caloric but changing protein intake in critically ill, ventilated, anuric patients on continuous renal replacement therapy and measuring amino acid and glucose losses across the hemofilter. METHODS: Eleven consecutive, critically ill patients (eight male, age, 43.5 +/- 21.8 y; Acute Physiology and Chronic Health Evaluation II score, 20.5 +/- 7.0; Acute Physiology and Chronic Health Evaluation risk of death: 36.5% +/- 23.0 and 6 +/- 1 impaired organ systems) entered this study. Patients were fed by continuous infusion of a total parenteral mixture consisting of Synthamin (a mixture of essential and non-essential amino acids), 50% dextrose, and intralipid (long-chain triglycerides) to meet caloric requirements as predicted by Schofield's equation corrected by stress factors. The amount of protein infused was varied (1 to 2.5 g. kg(-1). d(-1)) by increments of 0.25 g. kg(-1). d(-1). Patients were stabilized on each feeding regimen for at least 24 h before paired samples of blood and dialysate were taken for amino acid and glucose measurements. Continuous renal replacement therapy was performed by using a blood pump with a blood flow of 100 to 175 mL/min. Dialysate was pumped in and out counter-currently to the blood flow at 2 L/h. A biocompatible polyacrylonitrile hemofilter was used in all cases. RESULTS: With protein intakes below 2.5 g. kg(-1). d(-1), blood levels of 14% to 57% of the measured amino acids were below the lower limits of the normal range. At 2.5 g. kg(-1). d(-1), all measured amino acids were within the normal range. Amino acid balance became more positive as protein input increased (P = 0.0001). Glucose and amino acid losses were dependent on blood concentration. Overall, 17% (range, 13% to 24%) of infused amino acids and 4% of infused glucose were lost in the dialysate. CONCLUSIONS: This study of critically ill, ventilated, anuric patients on continuous renal replacement therapy suggested that increases in protein and glucose are required to account for the increased losses across the hemofilter. A protein intake of 2.5 g. kg(-1). d(-1) appeared to optimize nitrogen balance and correct amino acid deficiencies.     

Associations of renal function with polymorphisms in the delta-aminolevulinic acid dehydratase, vitamin D receptor, and nitric oxide synthase genes in Korean lead workers

We analyzed data from 798 lead workers to determine whether polymorphisms in the genes encoding delta-aminolevulinic acid dehydratase (ALAD), endothelial nitric oxide synthase (eNOS), and the vitamin D receptor (VDR) were associated with or modified relations of lead exposure and dose measures with renal outcomes. Lead exposure was assessed with job duration, blood lead, dimercaptosuccinic acid (DMSA)-chelatable lead, and tibia lead. Renal function was assessed with blood urea nitrogen (BUN), serum creatinine, measured creatinine clearance, calculated creatinine clearance and urinary N-acetyl-beta-D-glucosaminidase (NAG), and retinol-binding protein. Mean (+/- SD) tibia lead, blood lead, and DMSA-chelatable lead levels were 37.2 +/- 40.4 microg/g bone mineral, 32.0 +/- 15.0 microg/dL, and 767.8 +/- 862.1 microg/g creatinine, respectively. After adjustment, participants with the ALAD(2) allele had lower mean serum creatinine and higher calculated creatinine clearance. We observed effect modification by ALAD on associations between blood lead and/or DMSA-chelatable lead and three renal outcomes. Among those with the ALAD(1-2) genotype, higher lead measures were associated with lower BUN and serum creatinine and higher calculated creatinine clearance. Participants with the eNOS variant allele were found to have higher measured creatinine clearance and BUN. In participants with the Asp allele, longer duration working with lead was associated with higher serum creatinine and lower calculated creatinine clearance and NAG; all were significantly different from relations in those with the Glu/Glu genotype except NAG (p = 0.08). No significant differences were seen in renal outcomes by VDR genotype, nor was consistent effect modification observed. The ALAD findings could be explained by lead-induced hyperfiltration.     

Criteria for choosing amino acid therapy in acute renal failure.

Metabolic studies were performed on 19 patients with acute renal failure. Therapy included intravenous hyperalimentation using 15 to 20 g of essential amino acids or 20 to 40 g of essential plus nonessential amino acids and hypertonic glucose (37 to 50%). The effect of this parenteral feeding appears to be primarily pharmacological. Hypertonic glucose promotes the hyperinsulinemia important to be membrane function, the operation of the sodium pump, and cell metabolism. Administration of high biological value crystalline amino acdis potentiates the effect of insulin by inhibiting protein breakdown and promoting protein synthesis, particularly in muscle. This reduces tissue catabolism and urea formation, and promotes potassium, magnesium, and phosphate homeostasis. The branched-chain ketogenic amino acids valine, leucine, and isoleucine may be of particular importance. When indicated, administration of renal failure hyperalimentation and peritoneal or hemodialysis can be expected to complement each other and accelerate recovery. This intravenous fluid therapy, in turn, must be coordinated with proper hemodynamics, usually requiring a colloidal solution to maintain intravascular volume, and cardiotrophic agents such as digitalis and dopamine. Early use of renal failure can be expected to demonstrate the most striking response in terms of survival, early recovery from acute renal failure, and the preservation of physiological homeostasis.     

Nutrition disorders during acute renal failure and renal replacement therapy

The physiological and biological modifications related to acute renal failure in critically ill patients, including the current use of continuous renal replacement therapies, have dramatically changed the type and importance of the metabolic and nutrition disturbances observed during treatment of renal failure. This review summarizes the current knowledge and makes recommendations for the daily nutrition management of these patients. The filtration of water-soluble substances of low molecular weight by continuous hemodiafiltration results in significant losses of glucose, amino acids, low-molecular-weight proteins, trace elements, and water-soluble vitamins. The losses of these macronutrients and micronutrients should be compensated for. During continuous renal replacement therapy, the daily recommended energy allowance is between 25 and 35 kcal/kg, with a ratio of 60%-70% carbohydrates to 30%-40% lipids, and between 1.5 and 1.8 g/kg protein. Providing energy 25-35 kcal/kg/d with a carbohydrate/lipid ratio of 60-70/30-40 and protein 1.5-1.8 g/kg/d is recommended during continuous renal replacement therapy. Supplemental vitamin B(1) (100 mg/d), vitamin C (250 mg/d), and selenium (100 mcg/d) are also recommended.     

连续性血液净化与普通血液透析在老年急性肾衰竭患者中的对照研究

目的比较连续性血液净化(CBP)与普通血液透析(IHD)治疗老年急性肾功能衰竭(ARF)的疗效、预后及并发症。方法选取在某院就诊的老年急性肾衰患者38例,随机分为普通血液透析对照组和连续性血液净化治疗组,每组19例。对两组患者透析等综合治疗7 d、14 d、30 d的血清肌酐和尿素氮的水平,两组患者透析并发症情况、病死率情况等进行统计分析。结果两组并发症无明显的特异性及差异性,两组治疗方式对患者死亡率影响不具有统计学意义,CBP组,在治疗后7 d、14 d、30 d时,血清肌酐水平和尿素氮水平都低于IDH组,肾功能恢复较IDH组明显快。结论老年急性重症肾衰竭患者,应尽可能予以连续性血液净化治疗,促进肾功能恢复。