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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conservative management of chronic renal failure in children is essentially based on dietary prescription including recommendations for high caloric intake and a certain limitation of protein intake according to GFR in order to avoid any extra loading with nitrogen wastes. Prescriptions for sodium potassium and water have to be adjusted on their residual output. Prevention of osteodystrophy needs supplement of calcium, chelation of phosphorus with aluminium hydroxide and the prescription of vitamin D or its active derivatives. High blood pressure when present must be carefully controlled. Drugs, when necessary, have to be given with a dosage taking into account the level of renal failure. Finally, the mode of life of the uremic child should be as close to normal as possible.
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PMID:Conservative treatment of chronic renal insufficiency in children. 4 67

Hypercalcemia calls first for supportive measures, eg, adequate hydration, movement or mobilization of the patient to the greatest amount tolerated, and reevaluation of drugs being taken. When immediate lowering of the serum calcium level is not clinically mandatory, oral administration of furosemide, corticosteroid, or phosphorus should be considered. In acute emergencies, saline loading and parenteral furosemide therapy should be tried first, except in a patient with renal failure and congestive heart failure, in whom peritoneal dialysis or hemodialysis should be used instead. Calcitonin can be given for the first 12 to 24 hours to lower serum calcium concentration until a definitive management plan is formulated. Corticosteroid, if not contraindicated, should be started as soon as possible. In severe primary hyperparathyroidism with hypophosphatemia, phosphorus can be given intravenously until oral phosphate therapy can be established. Surgery, of course, should be performed as soon as possible. In most cases of neoplasia, mithramycin given according to a recommended schedule is safe and frequently effective. In desperate cases, additional use of prostaglandin synthesis inhibitors probably now is justified by empirical observations. All of these therapeutic measures are used only to stabilize electrolyte balance so that the primary cause of the hypercalcemia can be treated.
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PMID:Management of hypercalcemia. 15 84

Ninety-nine patients with end-stage renal failure treated by maintenance home dialysis whose calcium and phosphorus balance was carefully controlled were studied for radiographic evidence of hyperparathyroidism. A total of 43 showed evidence of hyperparathyroidism despite excellent medical management. In 23 the abnormality was stable and the patients were asymptomatic with regard to the skeleton. The other 20 showed progressive bone disease. Sixteen of these patients were operated upon, and 14 were relieved of their symptoms by parathyroidectomy. Following operation, the radiographic evidence of bone disease halted dramatically, and a decided return toward normal was documented on subsequent films. Thus parathyroidectomy can control the skeletal deterioration and bone pain of hyperparathyroidism in patients who develop this complication. Serial radiographic studies are a reliable indicator of this circumstance.
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PMID:Autonomous hyperparathyroidism in patients on maintenance home dialysis. 18 19

The discovery of the vitamin D endocrine system has opened up many possibilities in our understanding of metabolic bone disease. Of particular importance is the fact that we can now manage certain genetic disorders resulting in vitamin D-resistant rickets or vitamin D-resistant hypocalcemia with the new active hormonal forms of vitamin D and with intelligent dietary management to provide for correction of the mineral difficulty. Thus, in the case of vitamin D dependency, replacement need only be with the missing hormone, 1,25-(OH)2D3. On the other hand, familial hypophosphatemia requires adjustment of the plasma phosphorus by frequent administration of oral phosphate and the adjustment of intestinal calcium absorption by 1,25-(OH)2D3. Renal failure patients require the adjustment of plasma phosphorus concentration and parathyroid hormone status, and the administration of the missing hormone 1,25-(OH)2D3. Hypoparathyroid patients require oral calcium plus 1,25-(OH)2D3, and premature infants require administration of the 1,25-(OH)2D3 because the immature kidneys and immature parathyroid glands fail to produce the required amount of this hormone. Other vitamin D-resistant rachitic conditions cannot be discussed here for lack of space and for lack of information. Undoubtedly, such patients as those having rickets secondary to renal tubular acidosis and rickets secondary to hepatic disorders will eventually come under effecti dietary and hormonal management. In this sense, the vitamin D endocrine system and vitamin D-resistant rickets can serve as a prototype of management of a genetic disorder by dietary means.
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PMID:Vitamin D-resistant rickets. A prototype of nutritional management of a genetic disorder. 23 Sep 41

Infectious hematopoietic necrosis (IHN) is a rhabdoviral disease of rainbow trout (Salmo gairdneri). Trout were injected with IHNV, and various hematological and biochemical measurements of clinically ill fish were compared to uninfected controls. Infected fish had reduced corpuscular counts, hemoglobin, and packed cell volume, but normal mean corpuscular volume, mean corpuscular hemoglobulin, and mean corpuscular hemoglobin concentration. The percentage of immature erythrocytes was increased, but the percentage of leukocytes was unchanged. Differential leukocyte counts showed a significant decrease in neutrophils, increase in lymphocytes, but no change in monocytes. Unidentifiable necrobiotic cells were prevelant in blood smears and hematopoietic tissue imprints. Plasma bicarbonate, chloride, calcium, phosphorus, bilirubin, and osmolality were signigicantly reduced, but plasma glucose and anterior kidney ascorbate were unchanged. Plasma pH increased and the alpha fractions of the serum proteins were altered. No change was found in plasma enzymes, except that a LDH isozyme was significantly increased. The alkali reserve was diminished and alterations in acid-base and fluid balance occurred. Death probably resulted from a severe electrolyte and fluid imbalance caused by renal failure.
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PMID:Pathophysiology of infectious hematopoietic necrosis virus disease in rainbow trout: hematological and blood chemical changes in moribund fish. 23 12

Clearance studies were carried out in 18 non-oedematous patients with advanced renal failure (glomerular filtration rate less than 12 ml/min) to assess the diuretic effects of Bay g 2821 given different oral doses (120 mg to 360 mg). The results showed a significant increase in urinary volume and in clearances of sodium, calcium, magnesium, chloride, inorganic phosphorus and 51CrEDTA. There were no significant changes, however, in clearance of PAH, urea and uric acid. The diuretic response started in the first hour after drug intake, reached a maximum after 3 to 5 hours, and declined slowly in the following 3 to 4 hours. In patients with a glomerular filtration rate less than 3 ml/min the drug lost its effect. In rates between 5 to 10 ml/min the efficacy of Bay g 2821 was comparable to that of furosemide and ethacrynic acid. No side-effects were reported.
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PMID:Diuretic effects of Bay g 2821 in patients with advanced renal failure. 40 16

Trigonal-colonic anastomosis for diversion of urine into the colon was performed in 12 clinically normal dogs and in 10 incontinent dogs with diseases of the urinary bladder or urethra. Dogs were studied from 1 to 30 months after surgery. The surgical procedure was technically satisfactory. Fifteen of 22 dogs were studied with intravenous urography, and only 1 case of hydronephrosis was found. Pyelitis was a common histopathologic finding in both groups of dogs. Pyelonephritis developed in 30% of dogs, regardless of duration of anastomosis. Glomerular filtration rate was reduced in all dogs studied, but renal failure was infrequent. Values for blood urea nitrogen and serum inorganic phosphorus were elevated due to intestinal recycling of nitrogenous products and phosphate. Electrolyte imbalances were not a problem, but gastrointestinal disturbances developed in 3 of the 10 diseased dogs. Six of 10 diseased dogs survived from 9 months to more than 3 years. Trigonal-colonic anastomosis appears to be a satisfactory salvage procedure for incontinent dogs with diseases of the urinary bladder or urethra that do not respond to other forms of therapy.
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PMID:Trigonal-colonic anastomosis: a urinary diversion procedure in dogs. 44 50

A model of experimental renal osteodystrophy was established in the rats with chronic renal failure induced by partial nephrectomy and therapeutic effects of 1 alpha-hydroxyvitamin D3 (1 alpha-OH-D3) were studied. Male Wistar rats weighing 180 g were 5/6 nephrectomized and fed a normal diet (Ca and P : 1%) for 6 months. After the surgery, serum creatinine levels increased 60% and thereafter continued to rise gradually with their growth for 4 to 5 months, followed by rapid increase. The serum phosphorus levels were also elevated concomitantly and the serum calcium concentrations were normal. Marked bone resorption accompanied with hypertrophy of parathyroid glands was observed by histological examinations (Tetrachrome-Fuchsin stain, contact microradiography and H-E stain). The bone resorption seemed to be due to secondary hyperparathyroidism. Treatment with 0.25 micrograms/kg/day p.o. of 1 alpha-OH-D3 for 10 days in the uremic state resulted in remarkable new bone formation which was confirmed by histological examinations. These results clearly demonstrated that the reduction of nephron mass play a critical clue of renal osteodystrophy and 1 alpha-OH-D3 appears to have a good potential for clinical use in patients with renal failure and metabolic bone diseases.
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PMID:Effect of 1 alpha-hydroxyvitamin D3 in rats with experimental renal osteodystrophy. 46 52

An animal model was developed to examine the cause of resistance to the calcemic action of PTH in renal failure. Thyroparathyroidectomized (TPTX) rats were repeatedly reinfused with their excreted urine, over a 5-hour period, to produce an acute uremic animal with normal kidneys. Nonuremic controls were infused with equivalent volumes of a simple electrolyte solution. Using this model, we have demonstrated impaired calcemic response to PTH (Lilly Parathyroid Extract, 80 U/100 g) in urine-infused rats compared with electrolyte-infused rats. The final plasma calcium concentrations were 12.0 +/- 0.3 and 14.9 +/- 0.3 mg/dl, respectively (P less than 0.001). The cause of this impaired calcemic response was investigated by reinfusing rats with their own urine that had been pretreated with either activated charcoal or zirconium oxide in two different anionic forms, or urine that had been ultrafiltrated through an Amicon membrane of which the stated molecular-weight cut-off of the smallest pore-size membrane was 500 daltons. It was found that charcoal and ultrafiltration techniques had no effect, whereas the zirconium oxide treatment completely corrected the impaired calcemic response and returned the plasma phosphorus to a concentration similar to that in nonuremic controls. This can be explained by the fact that the principal effect of zirconium oxide on urine is to remove inorganic phosphate. Other groups of TPTX rats given PTH extract were infused with an electrolyte solution containing varying amounts of phosphate up to a maximum similar to the amount that a urine-infused rat would receive. A highly significant inverse relationship was found between the dose of phosphate infused with the electrolyte solution and the measured calcemic response to PTH. This relationship is represented by the following equation: calcium (mg/dl) = 14.84 - 0.139 inorganic phosphate; r = 0.915, P less than 0.001. From these series of studies, we conclude that phosphate retention is the cause of resistance to the calcemic action of PTH extract in this acute uremic model.
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PMID:Evidence that resistance to the calcemic action of parathyroid hormone in rats with acute uremia is caused by phosphate retention. 54 99

The progressive encephalopathy observed in 5 children with chronic renal failure was clinically similar to the so-called dialysis encephalopathy of adults, except that it was not related to dialysis therapy. Renal osteodystrophy is more prevalent in children than in adults and often more severe. The attempt to control the crippling deformities of renal osteodystrophy in growing children with renal insufficiency has led to the use of large quantities of aluminum containing antacids. The encephalopathy observed in children with chronic renal failure may be related to the oral ingestion of aluminum containing compounds in the presence of persistent secondary hyperparathyroidism. We suggest that alternative methods for the adequate control of serum phosphorus levels should be sought and indications for parathyroidectomy in children reevaluated. During the past 18 mos we have lowered the dose of aluminum containing compounds to 50 to 100 mg/Kg/day in our patients with progressive renal failure and recommend parathyroidectomy. No new cases of the encephalopathy have occurred.
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PMID:Encephalopathy in children with chronic renal failure. 61 6


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