Effects of reduced renal mass and dietary protein intake on amino acid release and glucose uptake by rat muscle in vitro.

Epitrochlearis muscles obtained from normal male Holtzman rats used as controls (C) and rats with reduced renal mass (Nx) fed isocaloric diets of varying protein content were incubated in Krebs-Ringer buffer containing 5 mM glucose for 1 or 3 h with or without insulin. Alanine (ALA) release rates from muscles of Nx rats were increased 40% above C values after 1 h of incubation regardless of protein intake. Addition of insulin decreased the ALA release from muscles of Nx rats to C values in animals fed 10 and 20% casein and chow but did not in rats fed 40% casein. After 3 h of incubation, all ALA release rates decreased by congruent with40%. The ALA release from muscles of Nx rats fed 10% casein was comparable to C values and decreased further with the addition of insulin. On the other hand, ALA release from muscles of Nx rats fed 20 and 40% casein as well as chow remained significantly elevated above C values, but responded to the addition of insulin with a reduction in release rates to C values, except from the muscles of Nx animals fed 40% casein. Tyrosine (TYR) and phenylalanine (PHE) release rates also were increased in muscles from Nx rats compared with C after 1 h of incubation. Release rates were highest in the Nx group fed 10% casein and decreased with increasing protein intake. Addition of insulin decreased the release rates of Nx rats to C values in each group. After 3 h of incubation, release rates of TYR and PHE in muscles from Nx rats remained significantly above C values for all groups, but responded to the addition of insulin with a decrease to C values. Glutamine and glutamate release were not significantly affected by reduction in renal mass.Base-line glucose uptake by all groups of muscles from Nx rats was significantly greater than corresponding C values, but maximal insulin-stimulated glucose uptake was comparable in all groups. Tissue pool sizes for glycogen, ATP, phosphocreatine, ALA, glutamate, and glutamine were unaffected by reduction in renal mass. The results indicate that Nx is associated with accelerated ALA, TYR, and PHE release from muscle. ALA release rose with increasing protein intake and decreased to values observed from C muscles after addition of insulin except in Nx animals fed 40% casein. TYR and PHE release decreased with increasing protein intake and also decreased to C values with the addition of insulin. The data also suggest that ALA release is not dependent upon glucose uptake in muscles from either C or Nx rats.

The relative roles of calcium, phosphorus, and parathyroid hormone in glucose- and tolbutamide-mediated insulin release.

The relative contributions of Ca++, phosphorus, and parathyroid hormone (PTH) on insulin secretion were evaluated in three groups of dogs. Dogs were studied with glucose infusions (group I) or standard intravenous glucose tolerance tests (IVGTT) (group II) before and after the development of diet-induced hypophosphatemia. Mean serum phosphorus levels for both groups fell from 4.1 to 1.1 mg/100 ml. Animals in group I demonstrated a fall in glucose disappearance rates (Kg) from 5.3+/-0.6% min to 3.5+/-0.5% after induction of hypophosphatemia (P less than 0.001). Mean insulin response was significantly greater in the hypophosphatemic animals than in controls in this group. In group II animals, mean insulin areas obtained during the IVGTT increased from 1,426+/-223 to 2,561+/-141 muU/ml/60 min after induction of hypophosphatemia, and were unaffected by Ca++ or PTH administration. Ca++ administration, but not hypophosphatemia or PTH infusion, increased significantly the mean insulin response to tolbutamide. Secondary hyperparathyroidism was induced by dietary manipulation in four dogs (group III). Mean PTH values increased from 71.4+/-2.1 to 3,012+/-372 pg/ml (P less than 0.001). Mean insulin response to an IVGTT was similar to group III animals, but increased from 1,352+/-128 to 1,894+/-360 muU/ml/60 min after the excessive dietary phosphorus was reduced for 3 mo, and plasma phosphorus fell from 3.2+/-0.1 to 2.8+/-0.3 mg/100 ml. PTH values decreased to 647+/-53 pg/ml. The insulin response to tolbutamide was comparable to that in group II animals, but increased significantly after calcium administration. Immunoreactive insulin disappearance rates were unaffected by hypophosphatemia or diet-induced secondary hyperparathyroidism. These data demonstrate that hypophosphatemia is associated with an augmented glucose-stimulated insulin release, without any effect on tolbutamide-stimulated insulin release. Hypercalcemia produces an augmented tolbutamide-stimulated insulin release with no apparent effect on glucose-stimulated insulin release. Finally, PTH does not appear to be an insulin antagonist and has no apparent effect on either glucose- or tolbutamide-stimulated insulin release in animals with dietary-induced secondary hyperparathyroidism.

Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients.

Current evidence suggests that administration of 1,25(OH)2D3 to patients with chronic renal insufficiency results in suppression of secondary hyperparathyroidism only if hypercalcemia occurs. However, since the parathyroid glands possess specific receptors for 1,25(OH)2D3 and a calcium binding protein, there is considerable interest in a possible direct effect of 1,25(OH)2D3 on parathyroid hormone (PTH) secretion independent of changes in serum calcium. Recent findings indicate substantial degradation of 1,25(OH)2D3 in the intestine, therefore, it is possible that while oral administration of the vitamin D metabolite increases intestinal calcium absorption, the delivery of 1,25(OH)2D3 to peripheral target organs may be limited. We therefore compared the effects of orally or intravenously administered 1,25(OH)2D3 on the plasma levels of 1,25(OH)2D3 and the effects of these two modes of treatment on PTH secretion. Whereas oral administration of 1,25(OH)2D3 in doses adequate to maintain serum calcium at the upper limits of normal did not alter PTH levels, a marked suppression (70.1 +/- 3.2%) of PTH levels was seen in all 20 patients given intravenous 1,25(OH)2D3. Temporal studies suggested a 20.1 +/- 5.2% decrease in PTH without a significant change in serum calcium with intravenous 1,25(OH)2D3. In five patients the serum calcium was increased by the oral administration of calcium carbonate, the decrement in serum i-PTH was only 25 +/- 6.65% when compared with 73.5 +/- 5.08% (P less than 0.001) obtained by the administration of intravenous 1,25(OH)2D3. Thus, a similar serum calcium achieved by intravenous 1,25(OH)2D3 rather than calcium carbonate has a greater suppressive effect in the release of PTH. These studies indicate that 1,25(OH)2D3 administered intravenously rather than orally may result in a greater delivery of the vitamin D metabolite to peripheral target tissues other than the intestine and allow a greater expression of biological effects of 1,25(OH)2D3 in peripheral tissues. The use of intravenous 1,25(OH)2D3 thus provides a simple and extremely effective way to suppress secondary hyperparathyroidism in dialysis patients.

Phosphate control and 25-hydroxycholecalciferol administration in preventing experimental renal osteodystrophy in the dog.

Previous studies from this laboratory demonstrated that secondary hyperparathyroidism in dogs with chronic renal disease may occur, at least in part, as a consequence of the need for progressive adaptation in renal phosphorus (P) excretion that occurs as glomerular filtration rate falls. However, the studies were of relatively short duration. Moreover, no information emerged regarding a potential role of calcium malabsorption in the pathogenesis of secondary hyperparathyroidism. The short duration of the protocol did not lend itself to the study of the effect of P control or the administration of vitamin D in the pathogenesis of renal osteodystrophy. In the present studies, 14 dogs with experimental chronic renal disease were studied serially for a period of 2 yr. Each animal was studied first with two normal kidneys on an intake of P of 1,200 mg/day. Then, renal insufficiency was produced by 5/6 nephrectomy. The dogs then were divided into three groups. In group I, 1,200 mg/day P intake was administered for the full 2 yr. In group II, P intake was reduced from the initial 1,200 mg/day, in proportion to the measured fall in glomerular filtration rate, in an effort to obviate the renal adaptation in P excretion. In group III, "proportional reduction" of P intake also was employed; but in addition, 20 mug of 25(OH)D(3) were administered orally three times a week. In group I, parathyroid hormone (PTH) levels rose throughout the 2-yr period reaching a final concentration of 557+/-70 U (normal 10-60). In group II, values for PTH remained normal throughout the 1st yr, increased modestly between the 12th and the 18th mo, but then did not rise after the 18th mo. In group III, no elevation of PTH levels was observed at any time; however, these animals were hypercalcemic. Histomorphologic analyses of the ribs of these dogs were performed serially throughout the 2-yr period. A linear relationship was obtained between the osteoclastic resorption surface and the concentration of circulating immunoreactive PTH. The osteoid volume was greater in group I animals when compared to those in group II. None of the morphologic abnormalities associated with renal osteodystrophy were observed in the animals in the third group.

Complications associated with arteriovenous fistulas in patients undergoing chronic hemodialysis.

Over a two-year period, 100 venous angiograms were performed on 75 patients because of difficulty with vascular access. Seventy percent of the patients had decreased arterial flow or increased venous resistance. High output failure, sepsis, and aneurysm formation were also found. Venous angiography of the fistula demonstrated significant stenosis in 40% of the cases as well as total occlusion by thrombus in 9%, aneurysm formation in 7%, and abnormal fistula needle placement or anatomic abnormalities in 20% of the cases. Definitive diagnosis with the aid of venous angiography permitted specific surgical intervention in 62% of the cases, and identified new sites for needle placement in 18% of the cases, thus prolonging fistula life and reducing the need for new fistula placement. Our experience with local cellulitis of the fistula site and sepsis is also discussed.

Upper gastrointestinal disease in chronic renal failure. A prospective evaluation.

A prospective study was undertaken to determine the incidence of upper gastrointestinal disease in 85 chronic renal failure (CRF) patients on hemodialysis. Upper gastrointestinal x-rays were obtained for 83 patients, and enlarged gastric and duodenal folds were seen in 12% (10/83) and 42% (35/83) of the cases, respectively. Panendoscopy performed on 60 persons revealed gastritis in 22% (13/60), nodular duodenitis in 60% (35/60), and esophagitis in 13% (8/60). No peptic ulcers were identified either radiologically or endoscopically. Pathologic examination of mucosal biopsy specimens demonstrated gastritis in 46% (21/46) and duodenitis in 43% (22/51) of patients. A highly significant correlation was found between endoscopic and radiologic duodenitis (P less than .0001) and also between endoscopic and pathologic duodenitis. We have demonstrated a high incidence of mucosal inflammation but not ulcer disease in CRF patients. These lesions may predispose these individuals to gastrointestinal bleeding following renal transplantation.

Cardiac failure and upper extremity arteriovenous dialysis fistulas. Case reports and a review of the literature.

Nine patients with high-output cardiac failure from arteriovenous forearm dialysis fistulas are reviewed, and six new cases are presented. Decreases in cardiac output with temporary fistula occlusion ranged from 0.3 to 11.0 liters/min (mean, 2.9 liters/min); fistula flow rates varied from 0.6 to 2.9 liter/min (mean, 1.5 liters/min). Surgical correction of high-flow fistulas resulted in notable improvement of cardiac failure in 13 of 14 patients. Although cardiac failure in individuals who are receiving long-term dialysis treatment is usually caused by intrinsic cardiac disease, volume overload, or anemia, forearm fistulas with large flow rates may be an important contributing factor. Correction of these large flow rates may be an important contributing factor. Correction of these large flow rates by banding or closure can substantially improve cardiac function in selected patients.

Does strict phosphorus control precipitate renal osteomalacia?

Hyperphosphatemia leads to the development of osteitis fibrosa in patients with chronic renal failure. In contrast, crippling osteomalacia may appear in uremic patients who are hypophosphatemic or aluminum intoxicated or who undergo total or subtotal parathyroidectomy. Thus, strict phosphorus control by use of aluminum-containing gels may ameliorate renal osteitis fibrosa, but may potentiate the development of osteomalacia. To evaluate this possibility, we compared the bone histologies of 10 chronic renal hemodialysis patients who consistently maintained predialysis phosphorus levels between 4-5 mg/dl (Strict-P) to those of 46 randomly selected dialysis patients (Random-P). We found that the Strict-P group had lower circulating immunoreactive PTH (P less than 0.02) and alkaline phosphatase (P less than 0.05) levels and, as expected, less evidence of hyperparathyroid bone disease. On the other hand, the Strict-P patients had osteomalacia, as evidenced by moderate osteoid accumulation and reduced capacity of bone to assume a fluorescent tetracycline label. Furthermore, all Strict-P patients had histological evidence of bone aluminum accumulation. We conclude that maintenance of normal serum P levels with aluminum-containing gels in hemodialysis patients prevents severe hyperparathyroid bone disease. Such treatment, however, is also attended by a moderate degree of aluminum-associated osteomalacia.

The metabolic and psychological effects of exercise training in hemodialysis patients.

The effect of exercise training on metabolic abnormalities and psychological function was assessed in seven hemodialysis patients. Their initial work capacity was low and improved after 8 months of training. Exercise was associated with a reduction in the dose of antihypertensive medications in four patients and a decrease in phosphate binder therapy in three patients. There was also a rise in hematocrit levels (% delta = 34 +/- 20%, P less than 0.03) and the hemoglobin concentration (% delta = 37 +/- 23%, P less than 0.05) of five males. Plasma glucose levels fell (-5 +/- 2%, P less than 0.05, n = 5) and the glucose disappearance rate improved (20 +/- 7%, P less than 0.02), while hyperinsulinism decreased (-36 +/- 20%, P less than 0.02, n = 5) during training. There was no change in body weight or diet. Exercise lowered plasma triglyceride levels (-41 +/- 28%, P less than 0.02, n = 6) and raised the high-density lipoprotein cholesterol concentration (20 +/- 21%, P less than 0.05, n = 6). Psychological testing (n = 4) demonstrated that exercise training was associated with an improvement in depression, hostility, anxiety, social interaction, and outlook for the future. These results suggest that exercise can improve some of metabolic abnormalities and psychological dysfunction which exists in some dialysis patients.

Comparison of the effects of prazosin versus propranolol on plasma lipoprotein lipids in patients receiving hemodialysis.

A prospective, crossover study was used to evaluate the effects of prazosin and propranolol on lipid metabolism in 10 hypertensive patients receiving long-term hemodialysis therapy. Adequate blood pressure control was achieved with either agent (mean predialysis blood pressure was 144/77 mm Hg). Total triglyceride levels increased by 27 +/- 4 percent during propranolol therapy but decreased during prazosin therapy by 8 +/- 2 percent (p less than 0.05). These changes were accounted for by a 21 +/- 1.5 percent increase in very-low-density lipoprotein triglyceride during propranolol therapy and a 6 +/- 2 percent decrease in very-low-density lipoprotein triglyceride during prazosin therapy (p less than 0.05). Although no change in total cholesterol occurred with either agent, a significant decrease (19 +/- 1 percent, p less than 0.01) in high-density lipoprotein cholesterol occurred with propranolol therapy and an increase of 16 +/- 4 percent occurred during treatment with prazosin (not significant). The high-density lipoprotein2 cholesterol levels decreased by 22 +/- 4 percent after treatment with propranolol and increased by 4 percent after prazosin therapy. Propranolol reduced high-density lipoprotein3 cholesterol levels by 18 +/- 2 percent, whereas prazosin increased these values by 19 +/- 2 percent (p less than 0.01). These changes were associated with a reduction in tissue lipoprotein lipase activity after propranolol therapy (2.4 +/- 0.3 percent) and an increase after prazosin therapy (2.5 +/- 1 percent, p less than 0.05). These data suggest that treatment with propranolol may be associated with unfavorable changes in the lipid profile that are not observed after treatment with prazosin.

Effects of prazosin and propranolol on blood pressure and plasma lipids in patients undergoing chronic hemodialysis.

Twenty patients receiving hemodialysis who had mild to moderate hypertension were treated with prazosin or propranolol to control predialysis hypertension. Effective blood pressure control was achieved with prazosin (mean dose 8.3 +/- 2.2 mg [+/- standard error of the mean], n = 10) and propranolol (mean dose 123 +/- 39 mg, n = 10). Therapy with prazosin did not significantly affect total plasma triglyceride or total cholesterol levels. The level of high-density lipoprotein (HDL) cholesterol tended to increase, but not significantly. However, the HDL3 subfraction did increase significantly, from 16.3 +/- 1.5 to 20.6 +/- 1.5 mg/dl (p = 0.05). Propranolol therapy increased plasma triglyceride levels, primarily of the very low density lipoprotein class. HDL cholesterol levels decreased from 44.2 +/- 6.7 to 34.7 +/- 4.2 mg/dl (p less than 0.03). The reduction in the HDL cholesterol levels was attributable to a decrease in HDL2 cholesterol levels (from 21.3 +/- 3.8 to 16.3 +/-3.0 mg/dl, p less than 0.04) and HDL3 cholesterol levels (from 23.0 +/- 3.1 to 19.5 +/- 2.1 mg/dl, difference not significant). Thus, both prazosin and propranolol are effective in controlling hypertension in patients undergoing hemodialysis. HDL3 cholesterol levels increased in patients treated with prazosin, but no other significant changes in the plasma lipids occurred. Patients treated with propranolol had a significant decrease in plasma HDL2 and HDL3 cholesterol levels.

Blood flow measurements in arteriovenous dialysis fistulas.

Blood flows were measured in 75 arteriovenous dialysis fistulas (AVF) at the time of fistula construction. End cephalic vein to side of radial artery AVF had a mean flow of 242 +/- 89 ml. per minute which was similar to bovine heterograft AVF that also originated from the radial artery (291 +/- 67 ml. per minute). AVF originating from the brachial artery had flow rates twice those originating from the radial artery (599 +/- 163 vs. 251 +/- 89 ml. per minute), respectively). Flow rates were similar for straight arm (641 +/- 111 ml. per minute), curved forearm (561 +/- 187 ml. per minute), and curved thigh (592 +/- 134 ml. per minute) bovine AVF. Initial blood flow through arteriovenous dialysis fistulas is too low to cause heart failure, except in patients with previously compromised cardiac function. In such patients AVF from the radial artery theoretically would be preferred over brachial or femoral artery AVF.

The indications for pericardiectomy in the uremic pericardial effusion.

Uremic pericarditis developed in 37 of 295 patients (8 percent) admitted to the chronic hemodialysis program at our institution. Sixteen patients (43%) underwent limited pericardiectomy through a left anterior thoracotomy approach with no operative deaths and minimal morbidity (19%). Twenty-one patients (57%) were treated successfully with intensive hemodialysis. The use of pericardiocentesis did not avert cardiac tamponade in any patient in our series. The procedure was associated with two life-threatening complications and its use, therefore, has been limited in the therapy of uremic pericarditis. We recommend surgical intervention in all patients with hemodynamic instability and echocardiographic evidence of enlarging effusions or an effusion unchanged in size following 10 days of intensive hemodialysis.

Abnormal cell-interactive properties of low-density lipoproteins isolated from patients with chronic renal failure.

Patients with renal failure on maintenance hemodialysis have accelerated rate of atherosclerosis. This, and the fact that chemically modified low-density lipoproteins (LDL) have a better capacity than native LDL to stimulate cholesteryl ester accumulation within macrophages in the vessel wall, led us to examine the possibility that some alteration in apo-LDL may take place in chronically uremic patients. We isolated LDL (d = 1.019 - 1.063 g/mL) from 18 patients with chronic renal failure and from 13 normolipidemic controls and compared the interactive properties of the different LDL preparations with cultured fibroblasts. Our results show that "uremic" LDL associates less, is degraded less, and has diminished ability to stimulate cholesteryl ester formation in fibroblasts when compared to normal LDL. LDL carbamylated in vitro showed interactive properties with fibroblasts similar to those of uremic LDL. Uremic LDL was not taken up by scavenger receptors present on rat peritoneal macrophages, similarly to normal LDL. However, the decrease in uptake by fibroblasts of uremic LDL may increase the residence time of these particles within the subendothelial region of the vessel wall, ultimately resulting in increased atherogenicity. Carbamylation of lysine residues of apoB in vivo, abnormal catabolism of LDL due to the absence of functional renal tissue, or triglyceride enrichment of LDL are among the possible explanations for the abnormal properties of uremic LDL.

Effects of exercise training on muscle protein catabolism in uremia.

The effects of exercise training on muscle protein catabolism in uremia were studied in female rats. Rats made uremic by 3/4 nephrectomy were compared with sham-operated control female rats under conditions of exercise training by swimming or no exercise. The release of amino acids from epitrochlearis muscle in vitro was measured. Body weight epitrochlearis muscle weight, and epitrochlearis protein content were similar among groups. Uremia increased the release of phenylalanine and tyrosine 33% and alanine 50% from muscle of sedentary rats. Citrate synthase activity and glycogen content of muscle were increased twofold by exercise in both controls and uremics. Exercise increased the release of alanine (60%), glutamine (50%), and pyruvate (30%) from muscles of control rats, but it decreased to control levels the release of phenylalanine and tyrosine in uremic rats. Alanine release remained elevated. To determine if exercise training increases in vitro muscle sensitivity to insulin, we incubated muscle with and without 0.01 U/ml of insulin. Phenylalanine and tyrosine release was reduced minimally by insulin in both sedentary uremic and control groups. Glucose uptake was enhanced by 55% in both groups. But in the exercised uremic and control groups, insulin reduced phenylalanine and tyrosine release by 50% and increased glucose uptake by 75%. These results suggest that exercise training reduces muscle protein catabolism in uremia; and this reduction is associated with enhanced muscle response to pharmacologic doses of insulin in control and uremic rats.

Therapeutic benefits of exercise training for hemodialysis patients.

Twenty-five hemodialysis patients were randomized into comparable exercising (E, N = 14) and sedentary control (N = 11) groups. After baseline testing, training was 3 to 5 times weekly for a mean of 12 +/- 4 (SD) months. Maximal aerobic capacity increased 21% (P less than 0.01), and the durations for the graded exercise stress test improved 19% (P less than 0.01) in E, but did not change in controls (8 +/- 4 months). Declining blood pressures in 8 hypertensive E led to reductions in antihypertensive medications; no changes occurred in 9 hypertensive controls. Exercise lowered plasma total triglyceride levels 33% (280 +/- 258 to 175 +/- 95 mg/dl; P less than 0.01), but no change occurred in total and low-density lipoprotein cholesterol concentrations. High-density lipoprotein cholesterol levels rose 16% in E (31 +/- 9 to 36 +/- 12 mg/dl; P less than 0.02), but did not change in controls. An increase in the affinity of insulin for receptors on mononuclear cells was associated with a 20% decrease in fasting plasma insulin levels (24 +/- 7 to 19 +/- 2 microU/ml, N = 8; P less than 0.05) and a 42% improvement in glucose disappearance rates (1.9 +/- 1.0 to 2.6 +/- 1.2% per min, N = 6) in E. There were no changes in the body weights or diets of the patients. A 27% increase in red blood cell mass (P less than 0.02) with no change in plasma volume resulted in a 27% increase in hematocrit (24 +/- 3% to 31 +/- 5%, P less than 0.01) and a 20% increase in hemoglobin (8 +/- 1 to 10 +/- 2 g/dl; P less than 0.01) in E.(ABSTRACT TRUNCATED AT 250 WORDS)

Endurance exercise training. An effective therapeutic modality for hemodialysis patients.

These results demonstrate that some of the metabolic complications of chronic uremia treated with maintenance hemodialysis are related to the deterioration in physical fitness and strength that accompanies this chronic disease. Exercise training increased the physical work capacity, improved the lipid profile, normalized insulin sensitivity and glucose metabolism, and lowered the dose of antihypertensive medications required by some of the patients. These changes occurred in the absence of significant changes in diet or body weight. Furthermore, during an equivalent period of follow-up there was a significant deterioration in the lipid profiles of sedentary controls. Thus, exercise training has the potential to reduce the prevalence of many of the medical conditions thought to promote atherogenesis in hemodialysis patients. In addition, there was a significant improvement in the degree of anemia of the exercising patients. None of these metabolic and physiological changes could be attributed to factors related to changes in dialysis scheduling or technology, medications, or diets. Exercise training was associated with an improvement in the mood, level of depression, and psychosocial functioning of these patients; the sedentary controls either became more depressed or reduced their participation in pleasant, socially oriented activities. This raises the possibility that exercise training may have the potential to return some dialysis patients to a more normal social lifestyle, perhaps improving their socioeconomic status and reducing their dependency. These are extremely optimistic possibilities that could have far-reaching implications for the hemodialysis population. The dramatic improvements in lipid and glucose metabolism, hematologic function, blood pressure and work capacity in the exercising patients indicates that aerobic physical training is an effective therapeutic modality with a wide spectrum of effects on many pathologic processes previously thought to be a consequence of chronic uremia. Not only were there major biochemical changes as a result of exercise training, but the psychosocial functioning of these dialysis patients improved. Some of the physiologic changes, such as the increase in work capacity, greater strength and energy, and the rise in hematocrit, contributed to the psychological improvements, but in some patients accomplishing the goal itself (for most a 1-mile jog was the ultimate) seemed sufficient. There are a multitude of potential long-term benefits of exercise training programs for hemodialysis patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Improving clinical processes: one dialysis facility's experiences.

Northeast Louisiana Dialysis Center implemented continuous quality improvement (CQI) to improve the quality of care delivered to end stage renal disease (ESRD) patients treated by hemodialysis in their facility. The unit chose to address normalization of calcium and phosphorus and parathyroid hormone (PTH), anemia, nutrition, adequacy of dialysis and dialyzer reuse as well as performance benchmarks by the Health Care Financing Administration (HCFA) core indicators. This article presents the results obtained and the methodology used in this improvement effort. The article also presents nine principles the authors believe necessary for a successful CQI program.

Acute renal failure. 1. Classification, evaluation, and clinical consequences.

Urinalysis and urine chemistries are most helpful in determining whether acute renal failure is due to a prerenal, renal, or postrenal cause. A plain film of the abdomen should be obtained, with ultrasound or computed tomography also being done if obstruction is suspected. When prerenal and postrenal causes have been excluded, the cause should be considered to be acute tubular necrosis, which progresses through initiating, oliguric (or sometimes nonoliguric), diuretic, and recovery phases. Acute tubular necrosis can produce a variety of clinical consequences affecting the entire body, including hyperkalemia, acidosis, hypocalcemia, anemia, and infection, as well as various cardiovascular, neurologic, and gastrointestinal problems.

Acute renal failure. 2. Pathophysiology, prevention, management, and prognosis.

During the past five years, much has been learned about the complex pathophysiology of acute renal failure. A number of mechanisms appear to be involved, including cell swelling, inhibition of prostaglandin synthesis, tubular obstruction, and disruption of the basement membrane of the proximal tubule. For patients at high risk of acute tubular necrosis, prophylaxis with mannitol or furosemide (Lasix) should be considered under certain circumstances. If this syndrome does occur, management should focus on maintenance of proper fluid and electrolyte levels and nutrition, which is facilitated by dialysis. The prognosis of acute tubular necrosis has changed little in the past ten years, and mortality remains high.