Protein catabolic rate may underestimate dietary protein intake in hemodialysis patients.
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Dietary Proteins↗
Biomedical subjects
J Uribarri
Publications and source records attributed to J Uribarri.
Past, present and future of end-stage renal disease therapy in the United States.
Dialysis was first described and used in 1854 to separate substances in aqueous solution based on different rates of diffusion through a semipermeable membrane. In vivo hemodialysis was performed in animals early in the twentieth century. Hemodialysis was first carried out in patients with acute renal failure in The Netherlands during the Second World War and in the United States in 1948. Repetitive hemodialysis for the treatment of chronic renal failure due to end-stage renal disease had to await the development of an acceptable long-lasting vascular access in 1960. The subsequent successful development of a technique to create an adequate arteriovenous fistula in 1972 permitted the rapid growth of dialysis programs, when the cost of this therapy was largely paid for by Medicare. Equipment has been developed to foster home-care hemodialysis and chronic ambulatory peritoneal dialysis. Enhancements in renal replacement therapy included the availability of recombinant human erythropoietin, calcitriol, and effective antihypertensive drugs. Technical advances in hemodialysis followed the use of bicarbonate dialysate, more biocompatible membranes, membranes of higher porosity, and ultrafiltration. Questions remain regarding the evaluation of the adequacy of dialysis which is to be achieved or prescribed. Careful attention to the management of the patient with progressive chronic renal insufficiency is crucial in dealing with the inevitable onset of uremia and the initiation of dialysis and/or renal transplantation. The cost of renal replacement therefore represents a great societal burden. A better understanding of how to prevent onset and progression of specific nephropathies along with the availability of new and more effective equipment for renal replacement therapy has a high priority.
Calcitriol↗
Caloric intake in a group of peritoneal dialysis patients.
Dialysis patients as a group appear to have a caloric intake less than the recommended values; because their energy expenditure is not different than that of healthy adults, they should be in negative caloric balance and lose body mass progressively. We retrospectively analyzed our data in a group of peritoneal dialysis patients who had dietary evaluations and kinetic measurements performed two consecutive times over a period of 6 months. Body weight, lean body mass (LBM), fat mass, and anthropometric parameters remained stable over this period of time, suggesting that these patients are not in negative energy balance. When their daily caloric intake was normalized to a new ideal body weight derived from the LBM calculated from creatinine kinetics, the values were within normal limits, suggesting that these patients were in zero energy balance; hence, a stable body mass was expected.
Adult↗
Middle molecule clearance does not influence protein intake in hemodialysis patients.
Nutritional status in hemodialysis patients is a strong predictor of morbidity and mortality. To isolate the impact of dialyzer flux on nutrition in hemodialysis patients, we compared the nutritional effect of high-flux dialysis with that low-flux dialysis, using a biocompatible membrane for both. Sixty-five patients were monitored for 8 months after changing to high-flux dialysis with a F80 polysulfone dialyzer following a 6-month baseline period of low-flux dialysis with a F8 polysulfone dialyzer. The Kt/V and normalized protein catabolic rate (nPCR) were the same on both the F8 and F80 dialyzers. The regression of nPCR versus Kt/V was also nearly identical. Despite the unchanged protein intake, the serum albumin (3.86 to 4.04 g/dL; P < 0.01) and serum creatinine (10.3+/-0.2 mg/dL to 11.2+/-0.3 mg/dL; P < 0.05) significantly increased during 8 months of high-flux dialysis. Therefore, we conclude that the increased removal of middle molecules by high-flux dialysis has no apparent effect on appetite as measured by nPCR, but it has a beneficial effect on serum albumin and serum creatinine, suggesting a role for middle molecules in the control of albumin and protein synthesis in the body.
Appetite↗
D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms.
This report describes a case of d-lactic acidosis observed by the authors and then reviews all case reports of d-lactic acidosis in the literature in order to define its clinical and biochemical features and pathogenetic mechanisms. The report also reviews the literature on metabolism of d-lactic acid in humans. The clinical presentation of d-lactic acidosis is characterized by episodes of encephalopathy and metabolic acidosis. The diagnosis should be considered in a patient who presents with metabolic acidosis and high serum anion gap, normal lactate level, negative Acetest, short bowel syndrome or other forms of malabsorption, and characteristic neurologic findings. Development of the syndrome requires the following conditions 1) carbohydrate malabsorption with increased delivery of nutrients to the colon, 2) colonic bacterial flora of a type that produces d-lactic acid, 3) ingestion of large amounts of carbohydrate, 4) diminished colonic motility, allowing time for nutrients in the colon to undergo bacterial fermentation, and 5) impaired d-lactate metabolism. In contrast to the initial assumption that d-lactic acid is not metabolized by humans, analysis of published data shows a substantial rate of metabolism of d-lactate by normal humans. Estimates based on these data suggest that impaired metabolism of d-lactate is almost a prerequisite for the development of the syndrome.
Acidosis, Lactic↗
Acid production in chronic hemodialysis patients.
This study examines endogenous acid production in a group of stable chronic hemodialysis patients with no residual renal function who were admitted to the chronic hemodialysis unit of Mount Sinai Hospital. Net acid production was estimated by the change in body bicarbonate content, which occurs in the interdialytic period. The body bicarbonate content at any time was measured by multiplying the concentration of blood bicarbonate by the apparent bicarbonate space at that time. The apparent bicarbonate space was determined by the change in blood bicarbonate concentration induced by the intravenous administration of a known amount of sodium bicarbonate. Daily sulfuric acid production was also estimated from the reduction in body sulfate content during dialysis. The interdialytic net acid production was measured at approximately 28 mEq/d, a value much lower than that predicted from the protein catabolic rate. This reduced acid production can be explained by reduced sulfuric acid and organic acid production. The mechanism of reduced sulfuric acid production is unknown. Reduced organic acid production is explained partly by the absence of renal excretion of metabolizable organic anions, leaving only the nonmetabolizable fraction as the main source of acid in the interdialytic period.
Acids↗
Normalization of protein catabolic rate to a new body weight derived from lean body mass in dialysis patients.
BACKGROUND: Since dietary protein is required for replenishment of lean body mass and since dialysis patients may have a significant increase in body fat, it makes sense to express protein intake normalized per lean body mass. However, this may be complicated since the daily protein requirements of man, based on studies done in the past with normal subjects, are usually expressed in grams of protein per kilogram of body weight. PATIENTS AND METHODS: We analyzed our data on urea and creatinine kinetics obtained in the routine clinical care of our peritoneal dialysis patients and calculated lean body mass from creatinine appearance rate. Using this lean body mass, we then reconfigured the patients' body to match the same proportion of lean body mass as in reference young men in which the initial recommendations for normal intake of protein were made. RESULTS AND CONCLUSION: We believe that this new theoretical body weight obtained by assuming that lean body mass always represents 85% of it may provide a more rational way to normalize daily protein intake.
Blood Urea Nitrogen↗
Moderate metabolic acidosis and its effects on nutritional parameters in hemodialysis patients.
We screened the laboratory data of all of our chronic hemodialysis patients to identify 2 groups: 1) those with a pre-dialysis total CO2 concentration equal or less than 21 mEq/l (group A) and 2) those with a pre-dialysis total CO2 concentration equal or greater than 25 mEq/l (group B) and then both groups were compared for the following parameters: protein catabolic rate, dietary protein intake by dietary history, Kt/V, serum albumin, weight, pre-dialysis serum creatinine and pre-dialysis BUN. Patients from group A had a significantly lower age, a significantly higher protein catabolic rate and significantly higher values for pre-dialysis serum creatinine and BUN. The values for body weight, dietary protein intake and serum albumin were also higher in group A than in group B but the differences did not reach statistical significance. There was a good correlation between protein catabolic rate and pre-dialysis total CO2 and between the latter and serum albumin. These results suggest that moderately low pre-dialysis serum bicarbonate concentration is usually the result of high protein intake and should be of no concern in well-dialyzed patients with a protein catabolic rate greater than 1 g/kg/day. However, further studies are needed to confirm this conclusion.
Acidosis↗
Acid-base balance in chronic peritoneal dialysis patients.
Endogenous acid production has never been measured directly in dialysis patients and an empiric formula is used to estimate acid production from their protein catabolic rate. We have studied acid-base balance in 19 stable CAPD patients attending the peritoneal dialysis clinic of Mount Sinai Hospital. They obtained a 24 hour collection of peritoneal dialysis fluid and urine while consuming their usual diet and performing their usual activities. Total alkali gain was calculated from net GI alkali absorption plus urinary net acid excretion plus alkali gain from dialysate, while total acid production was measured directly from the urinary and dialysate excretions of sulfate and organic anions. Net GI alkali absorption was estimated from the difference between cations (Na + K+Ca + Mg) and anions (Cl + 1.8P) in the 24 hour dialysate and urine collections minus the daily total amount of lactate infused. All of our patients had a normal or high serum bicarbonate concentration, which was stable with time. Total alkali gain was virtually identical to total acid production (54.2 vs. 52.4 mEq/day) which suggests that these patients were in neutral acid-base balance. Net GI alkali absorption (22.7 mEq/day) was one of the same range as that of chronic renal failure patients not on dialysis and represented almost one half of the total daily alkali gain. The daily acid production of 52.4 mEq/day was numerically equal to 84% of the protein catabolic rate expressed as g/day, which is similar to the predicted value of 77% of PCR reported in the literature.(ABSTRACT TRUNCATED AT 250 WORDS)
Acid-Base Equilibrium↗
A re-evaluation of the urinary parameters of acid production and excretion in patients with chronic renal acidosis.
We have studied acid-base balance in 32 patients attending the renal clinic of Mount Sinai Hospital. The parameters of acid-base balance measured included acid production measured as urinary sulfate and organic anions, net acid excretion measured as urinary ammonia plus titratable acid minus bicarbonate, and net GI absorption of alkali measured by a new method utilizing urinary electrolytes. Net GI absorption of alkali by urinary electrolytes measures alkali addition to the body from the GI tract as well as from any other sources, including bone. All patients had a creatinine clearance less than 80 ml/min and they were divided into two groups: those with normal serum bicarbonate (Group 1; N = 12) and those with subnormal serum bicarbonate (Group 2; N = 20). Hydrogen ion balance was -0.6 +/- 9 mEq/day in the first group, while those in the second group had a hydrogen ion balance of +16 +/- 5 mEq/day. A group of 8 normal controls had a hydrogen ion balance of -0.3 +/- 5 mEq/day. When the sum of all cations was compared with the sum of all anions in the urine, a cation gap of exactly the same magnitude as the positive hydrogen ion balance was found in patients with low serum bicarbonate. In conclusion, our data show that patients with decreased GFR and low serum bicarbonate appear to have a significantly positive hydrogen ion balance. However, we believe that the positive hydrogen ion balance is only apparent, but not real for the following reasons.(ABSTRACT TRUNCATED AT 250 WORDS)
Acid-Base Equilibrium↗
Peritoneal clearance of inorganic sulfate.
The peritoneal clearance of sulfate was studied in a group of 12 stable CAPD patients and compared to the clearance of other well-studied solutes such as urea, phosphate, and creatinine. For this purpose we obtained 24 h peritoneal dialysate collections and performed a modified 6-hour peritoneal equilibration test. The results showed that the peritoneal clearance of sulfate is very similar to those of creatinine and phosphate but significantly smaller than the clearance of urea. Decreased daily excretion of sulfate in relation to protein catabolic rate was noted and requires further studies to define its mechanisms.
Creatinine↗
Renal stone risk factors in patients with type IV renal tubular acidosis.
Renal stone formation is uncommon in patients with type IV renal tubular acidosis (RTA). This study was undertaken to explore the urinary biochemical and physicochemical factors in patients with type IV RTA in order to elucidate the mechanisms that protect them from renal stone formation. Twelve subjects with type IV RTA and 12 matched subjects with a similar degree of kidney impairment but without RTA were studied. Both groups of patients had low urinary excretion of calcium, phosphorus, uric acid, and citrate, probably reflective of kidney impairment. Patients with type IV RTA had a significantly lower urinary pH and urinary excretion of calcium than their matched controls. Hypocitraturia was present in both groups without any significant difference between them. This study suggests that the major protection from renal stone formation in type IV RTA results from impaired renal function and ensuing reduction in renal excretion of stone-forming substances, such as calcium and uric acid.
Acidosis, Renal Tubular↗
Serum albumin: associations and significance in peritoneal dialysis.
Hypoalbuminemia in hemodialysis patients is a strong predictor of mortality; however, the significance of hypoalbuminemia in peritoneal dialysis patients is less well-defined. We have analyzed the factors associated with hypoalbuminemia in a cross-sectional study of 36 peritoneal dialysis patients, and investigated the impact of hypoalbuminemia on the one-year clinical outcome in 53 peritoneal dialysis patients. We found hypoalbuminemia to be associated with low values for the kinetic parameters KT/V, creatinine clearance, and normalized protein catabolic rate (nPCR) by univariant analysis. In a multiple regression model, nPCR was the only significant predictor of serum albumin. Clinical outcome measures evaluated were days-hospitalized, peritonitis rate, and death. Days-hospitalized was inversely correlated with serum albumin, and deaths occurred only in patients with serum albumin less than 4.0 mg/dL. There were no associations with peritonitis episodes. In conclusion, our study provides evidence that hypoalbuminemia in peritoneal dialysis patients is associated with a low protein intake measured by the nPCR and, possibly, with a low delivered dose of dialysis. Our study also suggests that the serum albumin level correlates to clinical outcome measured by days-hospitalized.
Creatinine↗
Combined liver-kidney transplantation. For the genetic disorder primary hyperoxaluria type I.
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Adult↗
Renal hypouricemia and absorptive hypercalciuria: a real syndrome.
We describe a case of renal hypouricemia due to increased tubular secretion of urate associated with absorptive hypercalciuria. This association has been described in the past, but this is the first time that high plasma levels of 1,25-dihydroxyvitamin D have been reported. A possible cause-and-effect relation between altered uric acid transport and altered vitamin D metabolism in the proximal tubule is suggested.
Adult↗
Hereditary nephrogenic diabetes insipidus and bilateral nonobstructive hydronephrosis.
We describe 2 cases of hereditary nephrogenic diabetes insipidus with massive bilateral dilatation of the urinary tract without any organic obstruction. A review of the literature revealed that dilatation of the urinary tract was present in 67% of the reported cases of nephrogenic diabetes insipidus which included a description of the urinary tract. This strong association between hereditary nephrogenic diabetes insipidus and nonobstructive hydronephrosis suggests a cause-and-effect relationship in which polyuria is responsible for the hydronephrosis.
Adult↗
Altered water metabolism in tuberculosis: role of vasopressin.
PURPOSE: Patients with hyponatremia due to tuberculosis have shown variable responses to water loading in previous small studies, ranging from persistent antidiuresis to a normal diuresis. Although tuberculosis is considered a cause of the syndrome of inappropriate antidiuretic hormone secretion (SIADH), circulating vasopressin has been documented in only a few cases. We studied a larger group of patients to determine whether it can be suppressed by a short-term reduction in osmolality. PATIENTS AND METHODS: Twenty-eight hyponatremic patients (mean age +/- SD: 40 +/- 10 years) with pulmonary or miliary tuberculosis underwent a clinical evaluation, measurement of blood and urine chemistry values, and (in 22) a water load of 20 mL/kg. Volume status was evaluated by urine sodium concentration, blood and urine urea nitrogen, and plasma renin activity. Endocrine, renal, and other recognized causes of SIADH were excluded. RESULTS: All 22 patients exhibited a decline in urine osmolality and an increase in free water clearance after water loading. Water excretion was fully normal in seven of 22, with the remainder showing variable impairment of diluting ability and/or volume excreted. Plasma vasopressin, measured in 11 of 22 patients as well as in six others not subjected to water loading, was detectable despite hypo-osmolality in 16 of 17. Vasopressin levels declined after water loading, from 1.85 +/- 1.32 to 0.77 +/- 0.25 pg/mL (p less than 0.05). The majority of patients had the euthyroid sick syndrome but normal adrenal responses to cosyntropin. Although several patients had mild volume depletion when studied, this factor did not appear to explain the defect in water excretion. Hyponatremia resolved predictably within days to weeks of antituberculous therapy. CONCLUSIONS: Circulating vasopressin remains detectable in hyponatremic patients with tuberculosis and is responsive to changes in osmolality. A downsetting of osmoregulation induced by active tuberculosis ("reset osmostat") could explain this abnormality, but we cannot exclude an unidentified non-osmotic stimulus that can be counteracted by water loading.
Adult↗
Metabolic acidosis due to inapparent defects in renal acid excretion in a patient with chronic diarrhea.
In a patient with persistent diarrhea, renal acid excretion was examined because fecal alkali loss was insufficient to account for chronic metabolic acidosis. Bicarbonate wasting did not occur at physiologic serum concentrations, and the patient's ability to lower urine pH after an acid load was within normal limits. Glomerular filtration rate and the maximal rate of distal hydrogen ion secretion were unequivocally reduced, however, and ammonium excretion ws consequently inadequate. Unanticipated hypophosphaturia limited urinary titratable acidity. This case demonstrates that renal dysfunction may contribute significantly to acidosis associated with diarrhea and shows that defects in renal acid excretion may be superficially inapparent.
Acidosis↗