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

9 patients with advanced renal failure and renal osteodystrophy documented by iliac crest biopsy were treated with 1,25-dihydroxycholecalciferol (average dose 0.53 micrograms per day) for 6 months. Under 1,25-DHCC there was a statistically significant increase in serum calcium and decrease in serum alkaline phosphatase and immune parathyroid hormone. Histomorphometric evaluation of posttreatment bone biopsies showed reduction of osteoclastic resorption and endosteal fibrosis. Osteoid volume decreased in most cases. In 3 patients with predominant fibroosteoclasia, bone turnover practically normalized. Bone mineral content of the radius (photoabsorptiometry) did not change with treatment. Transient hypercalcemia occurred in 5 patients and was easily corrected by adjustment of 1,25-DHCC dosage.
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PMID:[Effect of 1,25-dihydroxycholecalciferol in renal osteopathy]. 53 67

Severe hypocalcemia secondary to magnesium depletion has been described in numerous patients with gastrointestinal disorders. The development of profound hypomagnesemia in chronic renal disease is a rare finding. We studied three patients with advanced renal failure and magnesium depletion. Severe hypocalcemia also was present in these patients. Despite hyperplasia of the parathyroid glands, the levels of immunoreactive parathyroid hormone (PTH) in blood were inappropriately low for the degree of renal insufficiency. After the administration of magnesium there was a significant increase in the levels of circulating i-PTH in serum with a concomitant improvement in the hypocalcemia.
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PMID:Hypomagnesemia and impaired parathyroid hormone secretion in chronic renal disease. 62 50

Neurological abnormalities are a major cause of morbidity in patients with renal failure. The pathophysiology of these neurological changes is unclear, and the effects on them of dialysis and return of renal function have not been well studied. Studies were done in 31 patients who had acute renal failure (ARF), all of whom were either treated with dialysis within 5 days or did not survive. Studies on these patients included the electroencephalogram (EEG), motor nerve conduction velocity, and plasma Ca(++) and parathyroid hormone (PTH) levels. Studies were done at the time ARF was diagnosed, after stabilization on dialysis, during the diuretic phase of ARF, and 3 mo after recovery from ARF. In 16 patients with acute or chronic renal failure who did not survive and in nine patients without renal disease who died, measurements were made in brain of content of Na(+), K(+), Cl(-), Ca(++), Mg(++), and water. In patients with ARF for less than 48 h, despite the fact that there were only modest increases in plasma urea and creatinine, there were striking abnormalities in the EEG. The percent EEG power < 5 Hz+/-SE was 41+/-8% (normal = 2+/-1%), whereas the percent of frequencies > 9 Hz was only 22+/-6% (normal = 62+/-3%). These changes were unaffected by dialysis, but became normal with return of renal function and remained normal at 3 mo follow-up. The motor nerve conduction velocity was unaffected by either ARF or dialysis. In patients with ARF, the brain Ca(++) was 46.5+/-3.2 meq/kg dry wt, almost twice the normal value of 26.9+/-1.0 meq/kg dry wt (P < 0.001). The plasma PTH level was 3.2+/-0.6 ng/ml (normal < 1.5 ng/ml, P < 0.01). The increased brain Ca(++) was not related to an increased plasma (Ca(++)) (PO(4) (---)) product (r(2) = 0.14, P > 0.05). There was a small but significant decrement in brain Na(+) (P < 0.05), but brain water, K(+), and Mg(++) were unaffected by ARF.Thus, in patients with ARF for less than 48 h, the EEG is grossly abnormal and there are elevated levels of PTH in plasma. The PTH appears to have a direct effect on the brain, resulting in an increased brain Ca(++) content. The EEG abnormalities are unaffected by dialysis, but they become normal with return of renal function and remain normal after 3 mo follow-up. Thus, PTH may be a major uremic toxin, demonstrating evidence for central nervous system toxicity when there are only minimal abnormalities of other biochemical markers of ARF.
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PMID:Neurodiagnostic abnormalities in patients with acute renal failure. 65 7

Renal osteodystrophy has many skeletal pathologic features, eg, fibroosteoclasia (osteitis fibrosa), osteomalacia, osteopenia, pseudofracture, cyst formation, and osteosclerosis. Many of these are caused by the secondary hyperparathyroidism that usually accompanies renal failure. Derangements in parathyroid hormone secretion, calcium and phosphate metabolism, and renal production of 1,25-dihydroxycholecalciferol (the most active form of vitamin D) are all interrelated and pathogenetic features of renal osteodystrophy. Types of abnormalities detected radiologically vary with patient age, type of management, and duration of hemodialysis, as well as with techniques and type of film used and interest of the radiologist. An x-ray film of the hands should always be made--it will show subperiosteal resorption in a large number of patients on dialysis. Prevention and management of renal osteodystrophy hinge on control of hyperphosphatemia and hypocalcemia.
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PMID:Renal osteodystrophy in end-stage renal failure. 71 29

Progression of renal failure, represented by rising serum creatinine concentrations, was correlated with progressive elevation of serum parathyroid hormone (PTH) concentrations in 23 children. A significant linear relationship was established. Despite normal serum calcium concentrations in 11 children receiving maintenance hemodialysis, circulating PTH concentrations were elevated after six months. Progressive deterioration with time occurred in all variables tested, at six-month intervals. These complications were reversible with kidney transplantation or treatment with 0.25 to 2 microgram/day of calcitriol for four to 20 weeks.
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PMID:Calcium and parathyroid disorders in children. Chronic renal failure and treatment with calcitriol. 76 89

Serum phosphorus concentrations are maintained within narrow limits in humans. In the extracellular fluid most of the phosphorus is present in the inorganic form and at the level of the glomerulus greater than 90% of PO4 is ultrafilterable. The kidney plays a key role in PO4 homeostasis. Micropuncture experiments have demonstrated that 60 to 70% of the filtered PO4 is reabsorbed in the proximal tubule; however, there is evidence that a significant amount of PO4 is reabsorbed in the distal tubule. Phosphate secretion probably plays a minor role in the overall renal regulation of phosphate. In normal individuals the amount of PO4 ingested plays a key role in the amount that ultimately will be excreted in the urine. The reabsorption of PO4 along the nephron is regulated by a series of factors of which parathyroid hormone is the most important one. Hyperphosphatemia is seen frequently in clinical medicine and by far, the most common cause is a decrease in urinary PO4 excretion secondary to renal failure. From the practical point of view, the most effective way to treat hyperphosphatemia is to decrease PO4 absorption in the GI tract by the use of PO4 binders.
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PMID:Hyperphosphatemia. 87 Feb 69

The blood levels of 25-hydroxyvitamin D (25-HCC) in 26 patients with nephrotic syndrome (proteinuria of 6.5 g/24 h +/- 0.8 SEM) ranged between 1 and 18.6 ng/ml (8.6 +/- 1.0 SEM). This value was significantly lower (P less than 0.01) than that in normal subjects (21.8 +/- 2.3 ng/ml) and patients with chronic renal failure (24.8 +/- 2.3 ng/ml). There was inverse correlation (P less than 0.01) between levels of 25-HCC and magnitude of proteinuria and a direct relation (P less than 0.01) with serum albumin. Reduction in proteinuria was rapidly followed by a rise in blood 25-HCC toward normal. Ionized calcium levels were low in 16 of 26 nephrotic patients irrespective of degree of renal failure. In four of seven nephrotic patients with normal renal function, ionized calcium levels were low and showed an inverse relation with levels of parathyroid hormone. These data show that patients with nephrotic syndrome have low blood levels of 25-HCC probably due to its loss in urine. This derangement is probably responsible for the disorders of calcium metabolism in nephrosis.
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PMID:Blood levels of 25-hydroxyvitamin D in nephrotic syndrome. Studies in 26 patients. 93 Dec 2

Quantitative bone histology (micromorphometry of undecalcified sections, analysis under polarized light; fluorescence microscopy with tetracycline double labelling) as well as serum and urinary chemistry (creatinine clearance, parathyroid hormone, ionized Ca, bone phosphatase, pH), were studied in 50 patients with incipient to advanced (glomerular filtration rate, 80 to 6 ml/min x 1.73 m2 renal insufficiency. In incipient renal failure, indirect evidence of parathyroid hormone excess was found in the skeleton (empty osteoclastic lacunae, woven osteoid). Osteoclastic surface resorption was abnormally high when GFR fell below 50ml/min x 1.73 m2. With the tetracycline double-labelling technique, a mineralization defect was demonstrable in many but not all patients.
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PMID:Bone histology in incipient and advanced renal failure. 94 Feb 74

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

Immunoreactive parathyroid hormone (iPTH) and 25-hydroxycalciferol (25(OH)D) serum levels were determined in 32 patients with renal osteopathy, they were correlated with the results of bone biopsy and other clinical parameters. iPTH was closely related to bone histology, it did not correspond to serum calcium and alkaline phosphatase, but the correlation to serum phosphate was statistically significant. 25(OH)D levels were not related to the histological findings of osteomalacia or increased bone resorption, while a correlation between the vitamin D metabolite and serum calcium could be observed. Since iPTH and 25(OH)D levels exhibited a significant correlation, an inhibitory effect of 25(OH)D on parathyroid gland function in renal failure was discussed.
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PMID:[Immunoreactive parathyroid hormone, 25-hydroxycalciferol and bone histology in renal osteodystrophy (author's transl)]. 94 Feb 99


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