Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen cases of lactic acidosis are reported: 7 phenformin treated diabetes, 5 cardiovascular diseases (2 myocardial infractions, 2 pulmonary embolisms, 1 heart failure). In 2 patients no etiology was found. Concomittant renal failure or liver diseases were found in respectively 9 and 4 cases. Patients presented the usual criteria of lactic acidosis: clinical, polypnea, severe hypotension (9/16), peripheral symptoms of shock (12/16), hypothermia (9/16), abdominal pain (9/16): biologically, acidosis (pH = 6,99 +/- 0,01, HCO3- = 5,9 +/- 1,5 mmol), hyperlactatemia (14,1 +/- 3,6 mmol/l) with hig lactate/pyruvate ratio (105 +/- 73), and anion gap (24,3 +/- 4,2 mmol/l). Sodium bicarbonate infusion was performed in all cases (2,5 to 42 mmol/kg). Few cases required volhemic expansion or furosemid induced diuresis. One patient was treated with extrarenal dialysis. 13 patients were alkalinised with less than 185% of estimated deficit measured from alkalin reserve: 12 died. 3 patients received 185% more than this deficit, associated with furosemid (1,8 to 12,5 mg/kg): only one patient died ten days after by casual disease, with lactatemia of 3,2 mmol/l. In spite of the small number of patients, these findings suggest that an early and massive alkalinisation, with large doses of furosemid, can improve the severe lactic acidosis prognosis.
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PMID:[Lactic acidosis and intensive care. 16 cases (author's transl)]. 23 77

The pathophysiology of albumin metabolism in uremia was investigated by turnover measurements in a large series of uremic patients, either on conservative management or on dialysis therapy. A total of 62 turnover studies were performed in patients on dietary treatment, divided into two groups according to the duration of the low protein diet: 35 subjects from 6 to 30 days, 27 subjects from 6 months to 5 years. Albumin catabolism and distribution were measured by the two-tracer technique (131I-albumin and 125I-iodide, simultaneously injected iv), while albumin synthesis was directly determined in 10 patients by the use of 14C-carbonate and 131I-albumin. Sixteen turnover studies were also performed in a group of end-stage uremics on dialysis therapy by a two-tracer procedure especially designed to determine albumin catabolism in the course of a single peritoneal or hemodialytic treatment. The main features of albumin metabolism observed in the patients on dietary management were: normal intravascular albumin mass, marked reduction of the extravascular and total albumin pools, with proportionally reduced catabolism. No significant turnover difference was found between the short-term diet group and the patients on low-protein diet from 6 months to 5 years. As to the uremics on dialysis therapy, catabolic rate of albumin was 3-fold increased in three patients showing clinical features of "hypercatabolism" in the early phase of uremia, or during relapse from it. Albumin turnover rate returned to normal when measured during clinical steady-state conditions. All these findings suggest that a marked body protein depletion exists in chronic uremia, and that dietary treatment per se is not responsible for such a depleted state. Instead, the depletion of protein stores observed in the steady phase of chronic uremia may have been originated by the exaggerated increased catabolism in the early phase of renal failure, not compensated by a proportional increase of the synthetic rate, due to both the state of uremic intoxication and to the reduced dietary protein intake during the early phase.
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PMID:The metabolism of human serum albumin in renal failure on conservative and dialysis therapy. 68 77

In rats with renal failure produced by excision of one kidney and infarction of large portions of the other kidney, given a low calcium, high phosphorus diet for 2-3 weeks, GFR was reduced by 80 percent, the fractional excretion of sodium increased from 7 to 23 percent, that of bicarbonate from 16 to 23 percent and that of water from 4 to 13 percent. Single nephron GFR in the remaining nephrons was nearly doubled and end-proximal TF/P(In) was depressed from 2.3 to 1.8, and proximal TF/P(HCO3) from 0.52 to 0.35, the latter figure corresponding to an increase of absolute proximal HCO(3) reabsorption from 1.7 to 3.5 nEq/min or from 2.8 to 3.2 Eq/L of single nephron glomerular filtrate. Acute parathyroidectomy had no influence on the fall of GFR or the rise of SNGFR in the remaining nephrons and failed to cause any significant changes in proximal tubular bicarbonate reabsorption. Parathyroidectomy, on the other hand, practically prevented the rise of the fractional excretion of sodium and of water and inverted the rise of the fractional excretion of bicarbonate to a fall. The data are interpreted to indicate that secondary hyperparathyroidism in renal failure impairs distal nephron bicarbonate and sodium reabsorption and, thus, contributes to the maintenance of sodium balance, but could possibly aggravate acidosis.
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PMID:A micropuncture study of HCO3 reabsorption by the hypertrophied proximal tubule. 73 50

Bicarbonate reabsorption was studied in dogs before and after induction of renal failure, produced by infarction of one kidney and removal of the contralateral kidney. Glomerular filtration rate and renal plasma flow decreased to 21 and 37% of control values, respectively. Fractional potassium excretion and fractional phosphate excretion increased significantly. Volume expansion resulted in a significant decrease of bicarbonate reabsorption in both control and uremic groups. At comparable levels of fractional chloride excretion, bicarbonate reabsorption was significantly higher in renal failure than in control animals. In the second group of dogs, following induction of renal failure, sodium bicarbonate was given orally in an amount sufficient to neutralize endogenous acid production. Bicarbonate reabsorption was again significantly higher than in control animals. Thyroparathyroidectomy had no effect on bicarbonate reabsorption. Absolute bicarbonate reabsorption and sodium reabsorption were lineraly related in control animals and in those in renal failure; the ratio of absolute bicarbonate reabsorption/abolute sodium reabsorption was significantly higher in renal failure than in control. These data demonstrate that renal failure is associated with enhanced bicarbonate reabsorption which is not related to the state of extracellular volume, the need to increase acid excretion or the concentrations of parathyroid hormone. These findings suggest that there are additional unknown factors controlling bicarbonate reabsorption in renal failure.
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PMID:Bicarbonate reabsorption in chronic renal failure. 94 Feb 81

We studied the effect of converting 100 established CAPD patients from aluminium- to calcium-based phosphate binders. After a follow-up of 1 year only 60% of patients remained on calcium carbonate. Hypercalcaemia was the major problem, with more than 40% of patients having a serum calcium in excess of 3.0 mmol/l. Several patients required hospitalization for symptomatic hypercalcaemia. Hypercalcaemia was more common in patients with normal serum parathyroid hormone concentrations (65 versus 25%, P less than 0.01). Serum phosphate control was better prior to commencing calcium carbonate when patients were treated with aluminium phosphate binders mean 1.71 +/- 0.15 mmol/l (SEM) than at the time of maximum serum calcium concentration, 1.81 +/- 0.25, P less than 0.05. This study does not confirm the findings of others, which have suggested that calcium carbonate is a safe and effective phosphate binder for patients with end-stage renal failure.
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PMID:Audit of the use of calcium carbonate as a phosphate binder in 100 patients treated with continuous ambulatory peritoneal dialysis. 838 46

Much interest is currently centered on the use of calcium acetate as a phosphorus binder in patients with renal failure. Therefore, this compound in subjects previously stable on calcium carbonate and undergoing high-efficiency hemodialysis with a dialysate calcium of 2.5 mEq/L was evaluated. Twenty subjects were switched from generic calcium carbonate to a single calcium carbonate preparation for a period of 2 months. This was followed by a phase (1 month) in which calcium acetate was substituted for calcium carbonate at a dose containing half the amount of elemental calcium. Subjects then continued calcium acetate for 6 months. It was found that calcium acetate allowed comparable control of immunoreactive parathyroid hormone, calcium, and phosphorus levels compared with calcium carbonate. This occurred with half the amount of elemental calcium ingested in the form of calcium acetate (349 +/- 25 versus 699 +/- 75 mmol/day; P less than 0.001). With this lower dose, the overall incidence of hypercalcemia was the same with each formulation. In the eight subjects concurrently receiving i.v. calcitriol, the incidence of hypercalcemia was significantly higher during the first month of calcium acetate compared with that in those not receiving this compound (P less than 0.05). Of those four subjects receiving the high dose of calcitriol (2 micrograms thrice weekly), all required either reduction in the dose or discontinuation of the drug. Thus, mineral metabolism could be controlled adequately with calcium acetate despite using half as much elemental calcium compared with calcium carbonate. This, however, did not result in a lower incidence of hypercalcemia, particularly in those receiving i.v. calcitriol.
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PMID:Calcium acetate as a phosphorus binder in hemodialysis patients. 139 13

The effects of a very low-protein diet (VLPD) supplemented with amino acids and ketoanalogues (KA) and with 1 g of calcium carbonate and 1000 IU of vitamin D2, were studied in 17 patients with advanced renal failure (GFR < or = 20 ml/min) over a period of one year. The protein intake was 0.3 g protein/kg body wt/day. Daily phosphorus and calcium intake were respectively 1,500 mg and 300 mg. Sequential bone densitometry was performed and bone histomorphometry after double tetracycline labeling was evaluated, before and after one year of diet. Calcium and phosphate metabolism parameters were monitored every two months. In spite of a significant decrease of GFR, phosphorus, parathyroid hormone (1-84) and osteocalcin plasma levels decreased significantly, while low plasma bicarbonate normalized, and calcitriol and calcium levels remained respectively low and normal. Before the diet, histological study disclosed four cases of mixed osteopathy: osteomalacia associated with osteitis fibrosa (OM/OF), nine pure osteitis fibrosa (OF) and four with normal bone remodeling (NB). After one year of diet, the OM component of OM/OF disappeared, as evidenced by a normalization of the mineral apposition rate and osteoid thickness. In the patients presenting pure OF, a significant decrease in osteoblastic and osteoclastic surfaces, in the number of osteoclasts, and in the bone formation rate (BFR) were found. Vertebral mineral density measured by quantitative computerized tomodensitometry did not change significantly. In conclusion, this study not only confirms the beneficial effects of VLPD + KA + calcium on uremic hyperparathyroid bone disease in advanced renal failure assessed using static bone histomorphometry, but also shows a correction of histodynamic bone parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ketodiet, physiological calcium intake and native vitamin D improve renal osteodystrophy. 145 6

Recent interest in the role of oral calcium carbonate and low calcium dialysate has emphasised the need for a simple, safe and inexpensive test of intestinal calcium absorption. The stable, non-radioactive, strontium absorption test fits these requirements. Stable strontium and calcium-45 were administered simultaneously to 19 fasting CAPD patients and their serum levels were subsequently measured. There was a close correlation between the absorption of calcium and strontium at both 60 and 120 min post-ingestion. The two markers resulted in the same classification of patients as normal or malabsorbers in 18 of 19 cases (95%), suggesting that strontium could be substituted for calcium-45 in a 60-min test of absorption enabling safe, simple and repeated measurements in renal failure patients.
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PMID:Use of oral stable strontium to provide an index of intestinal calcium absorption in chronic ambulatory peritoneal dialysis patients. 146 51

Control of phosphorus accumulation in chronic renal insufficiency is crucial to the prevention of secondary hyperparathyroidism and metastatic calcification. In early renal failure, calcitriol levels are normal and parathyroid hormone levels are elevated. The phosphorus levels are maintained in the normal range by the phosphaturia induced by hyperparathyroidism. In this situation, dietary phosphorus restriction increases calcitriol levels and suppresses parathyroid hormone secretion. As renal failure progresses into late stages, hyperphosphatemia is evident along with low levels of calcitriol and worsening hyperparathyroidism. Phosphorus restriction will not affect calcitriol concentrations, yet parathyroid levels may decline. During long-term dialysis, urinary excretion of phosphorus is usually minimal. Therefore, phosphorus balance is determined primarily by the net amount absorbed by the bowel and the quantity removed during dialytic therapy. Given an adequate diet, no form of conventional dialysis is able to fully compensate for the gastrointestinal absorption of phosphorus. Hence, compounds that bind phosphorus in the bowel are often necessary. With the realization that the use of phosphorus binders containing aluminum leads to aluminum accumulation and its sequelae: osteomalacia, dementia, myopathy, and anemia, other phosphorus binders have been evaluated. Calcium carbonate has been investigated the most thoroughly and is in wide use. It is inexpensive and contains a high percent of elemental calcium. However, it is only modestly potent in the binding of phosphorus, and large doses are often necessary to attain satisfactory control of phosphorus. This may lead to hypercalcemia. One approach to this problem is to decrease the concentration of calcium in the dialysate. Alternatively, a more effective phosphorus binder may be used. Calcium acetate has been shown in acute studies to have twice the binding capacity of phosphorus per calcium absorbed than calcium carbonate. Whether use of this compound decreases the incidence of hypercalcemia is unproven. Calcium citrate increases the gastrointestinal absorption of aluminum and offers no advantage over calcium carbonate. Other compounds, such as calcium ketoacids and calcium alginate, have not been extensively studied and are not generally available. The use of phosphorus binders containing magnesium in conjunction with a dialysate low in magnesium may be efficacious. Large doses of magnesium will cause diarrhea and thus limit its use as a single agent. Reasons for failure to control hyperphosphatemia include poor compliance, improper prescription of binders, poor dissolution rates seen with some generic brands of calcium carbonate, and the presence of severe hyperparathyroidism. Optimal control of serum phosphorus in dialysis patients should always be viewed in the context of adequate nutrition and protein intake.
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PMID:Hyperphosphatemia: its consequences and treatment in patients with chronic renal disease. 156 18

Gastric conduit urinary diversion was performed in 10 dogs after complete cystectomy. Four dogs were euthanatized on day 30 because of hypochloremic metabolic alkalosis and renal failure. Hematologic and biochemical changes in six dogs evaluated for 120 days were compatible with hypochloremic metabolic alkalosis. The continuous loss of hydrochloric acid from the gastric conduit resulted in significant increases in arterial blood pH, PaCO2, anion gap, TCO2, and the concentration of HCO3-. There were significant decreases in PaO2 and the serum concentrations of chloride and potassium. Deterioration of renal function resulted in all dogs. It was concluded that hypochloremic metabolic alkalosis makes gastric conduit urinary diversion unsatisfactory for clinical use in dogs.
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PMID:Gastric conduit urinary diversion in normal dogs. Part II, Hypochloremic metabolic alkalosis. 158 55


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