Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with chronic renal failure (CRF) (CCr less than 20 ml/min), we have previously demonstrated greater rates of Na excretion (ex) when Na intake was nearly all NaHCO3 as compared to NaCl (both 200 mEq Na daily). Chloride (Cl) wasting on NaHCO3 (with severe Cl restriction) occurred, however, and may in part explain the results. To avoid Cl restriction in 6 patients with CRF (CCr 10-15 ml/min) on an estimated 10 mEq Na and Cl diet, electrolyte ex was compared on NaCl supplements of 200 mEq/day versus a daily mixture of NaHCO3 (100mEq) and NaCl (100 mEq). Periods on NaCl and the mixture lasted 4 days (order randomized) separated by re-equilibration to baseline weight (wt). Mean +/- SEM ex of Na, Cl, HCO3 mEq/day and CCr and deltawt (lbs) are compared below for the 4th day of NaCl vs NaHCO3 intake. (see article). Also there were no significant differences in K excretion, blood pressure, or plasma renin activities. Mean serum HCO3 increased from 21.2 to 25.8 mEq/l (day 1 vs 5, P less than 0.01) reflecting the net positive HCO3 balance on the mixture indicated above. Thus increments of Na intake above a fixed NaCl intake were excreted similarly whether given as NaCl or NaHCO3. Greater Na ex on NaHCO3 may depend on severe Cl restriction and/or higher serum HCO3 levels. If dietary NaCl intakes are near maximum tolerance, NaHCO3 supplementation should be accompanied by reductions in NaCl intake to maintain Na balance,
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PMID:NaHCO3 and NaCl tolerance in chronic renal failure II. 83 32

A patient is reported whose illness was characterized by chronic renal failure associated with persistent salt-wasting, chronic nephrolithiasis, and candiduria which was documented to be arising from the upper urinary tract. Intravenous amphotericin B was effective in eradicating candiduria. However, bilateral nephrectomy was ultimately performed which revealed extensive involvement of the renal parenchyma with classic caseating granulomas apparently related to renal candidiasis. Severe medullary erosion and tissue loss existed which appeared to result in disproportionate medullary destruction which was probably the most significant factor in explaining the patient's salt-losing state. The patient has since been satisfactorily managed with maintenance hemodialysis.
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PMID:Primary renal candidiasis with renal granulomata and salt-losing nephropathy. 113 Apr 31

In patients with chronic renal failure, NaHCO3 therapy may correct or prevent acidemia. It has been proposed that the NaHCO3 required will not result in clinically significant Na retention comparable to that from similar increases in NaC1 intake. In each of ten patients with chronic renal failure, creatinine clearance (Ccr) range 2.5-16.8 ml/min, on an estimated 10-meq Na and C1 diet, electrolyte excretion was compared on NaHCO3 vs NaC1 supplements of 200 meq/day. Periods of NaHCO3 and NaC1 (in alternate order for successive patients) lasted 4 days, separated by reequilibration to base-line weight. Mean +/- SEM excretion (ex) of Na, C1, and HCO3 and deltaCcr and deltaweight (day 4-1) are compared below for the 4th day of NaC1 vs. NaHCO3 intake. Mean Ccr +/-SEM on day 4 of NaC1 and NaHCO3 were 10.8 +/-1.6 and 9.0 +/-1.4 ml/min, respectively (P less than 0.02). Mean systolic blood pressure (but not diastolic) increased significantly on NaC1 (P less than 0.05). No significant blood pressure changes were seen on NaHCO3. Net positive HCO3 balance occurred on NaHCO3 as indicated above and reflected a rise in mean serum HCO3 from 19 to 30 meq/liter (day 1 vs. 4) (P less than 0.01). Mechanisms for the greater excretion of Na on NaHCO3 may relate to C1 wasting as noted above on low C1 intake and limited HCO3 reabsorptive capacity. Thus, Na excretion by day 4 was greater on NaHCO3 than on NaHCO3 did Na excretion near intake (210 meq/day).
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PMID:NaHCO3 and NaC1 tolerance in chronic renal failure. 115 Aug 79

Since the development of recombinant DNA technology, there has been a rapid expansion of research concerning the use of recombinant DNA synthesized human growth hormone (rhGH) for the treatment of clinical disorders. rhGH has been used to treat patients with acute catabolic stress caused by surgery, trauma and sepsis, children with chronic renal insufficiency and impaired growth, patients undergoing maintenance hemodialysis who are malnourished, and individuals on weight reduction diets. These studies indicate that rhGH enhances protein balance in acutely stressed patients and in malnourished maintenance hemodialysis patients, promotes catch-up growth in children with chronic renal failure, and may reduce protein wasting and enhance lipolysis in obese individuals on weight reduction diets. Experimental studies suggest that in addition to enhancing anabolism, rhGH may increase both immune function and the rate of wound healing. Many, but not all, of the effects of rhGH are mediated through insulin-like growth factor I (IGF-I). For example, the hyperglycemic and lipolytic effects of rhGH do not seem to be caused by IGF-I. Animal or human studies suggest that with severe malnutrition or severe sepsis, rhGH treatment may neither increase serum IGF-I levels nor promote anabolism. These observations provide a rationale for administering IGF-I as an anabolic hormone for severely malnourished or septic patients with renal failure. Further studies will be necessary to examine both the short-term and long-term potential benefits and adverse effects of rhGH or rhIGF-I treatment in these conditions.
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PMID:The rationale for the use of growth hormone or insulin-like growth factor I in adult patients with renal failure. 146 73

To maintain nitrogen equilibrium when prescribed a low protein diet (LPD), metabolic adaptations occur involving a reduction protein turnover, principally decreased muscle protein degradation. Studies suggest that in patients with chronic renal failure (CRF) uncomplicated by metabolic acidosis (MA), these adaptive responses are intact. Because MA stimulates muscle proteolysis, this study examined the hypothesis that in CRF complicated by MA, the adaptation to LPD may be impaired, inducing a nitrogen wasting state. Six adults with CRF (mean GFR: 12.8 +/- 1.5 ml/min) and MA (mean serum bicarbonate: 17.0 +/- 1.0 mM/liter) receiving an unrestricted diet (protein intake: 1.2 g/kg body wt/day) were converted to an isocaloric LPD (protein: 0.6 g/kg body wt/day). Two weeks later total urinary nitrogen losses decreased, but skeletal muscle protein catabolism (SMPC), assessed from the urinary 3-methyl histidine:creatinine ratio, increased, demonstrating impairment in the adaptive down-regulation of SMPC. The LPD was continued for a further two weeks and MA was corrected with oral sodium bicarbonate (mean serum bicarbonate: 24.3 +/- 1.2 mM/liter). Correcting MA decreased SMPC to a level below that measured prior to protein restriction. The decreased SMPC was paralleled by further decreases in urinary nitrogen losses, confirming that MA impaired nitrogen utilization. It is concluded that MA can override the expected metabolic adaptive response to a LPD. The associated impairment of nitrogen utilization not only diminishes the efficacy of the diet, but also accelerates the loss of lean body mass.
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PMID:Metabolic acidosis and skeletal muscle adaptation to low protein diets in chronic uremia. 174 30

Energy metabolism was measured by indirect calorimetry in 86 patients with various forms of renal failure and in 24 control subjects. In patients with acute renal failure with sepsis, oxygen consumption, carbon dioxide production, and resting energy expenditure were increased (P less than 0.05). In other groups with renal failure (acute renal failure without sepsis, chronic renal failure with conservative treatment or hemodialysis, and severe untreated azotemia) these indices were not different from those of control subjects. Urea nitrogen appearance was decreased in patients with chronic renal failure undergoing conservative treatment, in those with severe untreated azotemia, and in hemodialysis patients (P less than 0.05). We conclude that renal failure has no influence on energy expenditure as long as septicemia is absent. Reduced urea nitrogen appearance rates in chronic renal failure are due to a reduced energy and protein intake. Wasting is a consequence of decreased food intake but not of hypermetabolism in chronic renal failure.
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PMID:Energy metabolism in acute and chronic renal failure. 205 69

Loss of lean body mass occurs frequently in patients with acute or chronic renal failure, but the mechanism(s) causing this abnormality are unknown. Using animal models of experimental uremia, it was found that excess lactate formation in muscle is directly related to the rate of protein breakdown. This suggests that abnormal energy metabolism may be one mechanism for protein wasting. A second mechanism involves metabolic acidosis. Metabolic acidosis activates the catabolism of protein and amino acids in muscle of uremic rats independently of azotemia. Defects in sodium transport by Na,K-ATPase and the Na/K/Cl cotransport system suggest that intracellular ions including hydrogen may be abnormal. If this were the case, uremia would increase the susceptibility to the catabolic effect of metabolic acidosis.
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PMID:Protein and amino acid metabolism in uremia: influence of metabolic acidosis. 263 59

Loss of protein stores, reflected by negative nitrogen balance and accelerated accumulation if nitrogenous breakdown products, is an important factor in the morbidity of chronic renal failure and the high mortality rate of acute renal failure. Low protein intake intensifies the suppressed protein synthesis that results from impaired insulin-stimulated protein anabolism. The metabolic acidosis of uremia contributes to tissue loss, both by increasing muscle protein degradation, and by raising the requirements for essential amino acids. Correcting metabolic acidosis improves the nitrogen balance and reduces tissue wasting. It is important to ensure adequate nutrient intakes, rather than the low protein diet often prescribed to slow loss of renal function.
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PMID:Review: mechanisms for abnormal protein metabolism in uremia. 267 57

Patients with chronic renal failure are prone to develop negative nitrogen balance resulting clinically in wasting and malnutrition. To study the role of glucocorticoids in the pathogenesis of uremic catabolism, we determined urinary excretion rates of urea and Nt-methylhistidine in chronically uremic rats with and without RU 38486, a potent antiglucocorticoid. In comparison to pair-fed non-uremic animals, chronically uremic rats displayed significantly enhanced ureagenesis, as demonstrated by increased urinary urea excretion, and myofibrillar protein breakdown, as indicated by increased excretion rates of urinary Nt-methylhistidine. The administration of RU 38486 to chronically uremic rats, however, did not result in a normalization of urinary excretion of Nt-methylhistidine. Similarly, the antiglucocorticoid did not influence the extent of ureagenesis in our uremic animals, as it was demonstrated by comparable levels of urinary urea excretion. This suggests that glucocorticoids are not involved in the pathogenesis of enhanced catabolism in chronic renal insufficiency.
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PMID:Independence of enhanced protein catabolism from glucocorticoids in chronically uremic rats. 281 69

In 44 adult patients, 16 men and 28 women, with chronic renal failure who were dialysed under uniform conditions (Dialyser area 1.2 m2, blood flow 200 ml/min, dialysate flow 500 ml/min, dialysis fluid acetate concentration 35 mmol/l) we determined the plasma acetate concentration after 1 h of haemodialysis (1H-Ac) and 3 h of dialysis (3H-Ac). 1H-Ac was significantly lower than 3H-Ac in both male and female patients, and both mean values were significantly greater in males than in females. 3H-Ac showed a negative correlation with body surface area, serum creatinine before dialysis, and serum albumin, respectively. Using multivariate analysis, body surface area and serum creatinine showed the strongest significant combination of independent variables (R = 0.66), and accounted for 43% of the total variance in 3H-Ac. Sex, age, serum albumin and haematocrit did not further contribute to explaining the variance in 3H-Ac independently of body surface area and serum creatinine. Assuming that serum creatinine to some extent reflects the generation rate of creatinine and thus the muscle mass of the patients, our findings suggest that the rate of metabolism of acetate is proportional to the body size and that acetate is metabolised to a large extent in skeletal muscle. Accordingly, malnutrition with muscle-wasting may lead to slow metabolism of acetate and possibly to exaggerated acetate-related side-effects.
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PMID:Patient-related factors influencing the plasma acetate concentration during haemodialysis. 312 53


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