Gene/Protein Disease Symptom Drug Enzyme Compound
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 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with chronic renal failure and total diversion of the lower urinary tract have been considered poor transplant candidates, and post-transplant urinary diversion, i.e., Bricker loop, has been thought to be necessary. Our experience with nine patients clearly indicates that these patients are actually excellent transplant candidates and that post-transplant urinary diversion rarely is necessary. Ureteroneocystostomy of the allografted ureter was performed in seven patients with pretransplant total urinary diversion and all have completely normal bladder and renal function 10 to 66 months after transplantation; the two patients with Bricker loop procedures performed at transplantation died 7 months after transplantation of rejection and pancreatitis. The excellent results achieved with ureteroneocystostomy are attributed to (1) errors in diagnosis resulting in inappropriate bladder or ureteric surgery early in the course of the patient's disease; (2) confusion of immunologic of functional disorders with anatomic problems; (3) growth and development of the bladder, and (4) complete control of chronic bladder infection by pretransplant nephrectomy, ureterectomy, and antibiotics.
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PMID:Renal transplantation in patients with urinary tract abnormalities. 76 10

With the purpose of establishing the clinicopathologic correlation in pyelonephritis and to discard other interstitial nephrites, with present day morphologic criteria we analysed 63 casos that had been diagnosed as pyelonephritis, following Weiss and Parker's histologic criterion. The clinicopathologic diagnosis of pyelonephritis was confirmed in 12 cases; all of them showed obstructive uropathy and in most of them, there was chronic renal failure. Interstitial nephritis was established in 27 cases, all of them showing septicemia and almost half of the cases showed acute renal failure. Other 20 cases showed tubulointerstitial nephritis secondary to different types of glomerulopathies, fetal glomerulosclerosis, dysplasias, nephrophthisis, radiation nephritis and renal infarct. In 4 cases, the study of sections finer than the original, showed absence of histopathologic lesions. The results of the present study point out the main causes of confusion with the pathological diagnosis of pyelonephritis, the necessity to investigate predisposing uropathy in patients with urinary infection and stresses the importance to establish correlation with clinical and laboratory findings in cases with tubulointerstitial lesions.
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PMID:[Pyelonephritis and bacterial tubulointerstitial nephritis]. 125 17

Considerable confusion arises in defining osteomalacia in the presence of renal disease. There are no radiographic or biochemical features which satisfactorily identify all patients with osteomalacia. Histological definitions need to distinguish increased amounts of osteoid due to defective mineralisation from that due to increased bone turnover, both of which may coexist in chronic renal failure. The pathogenesis of osteomalacia in renal failure is multifactorial and not always due to defective metabolism of vitamin D. Deficient production of 25-hydroxyvitamin D may occur because of nutritional privation or urinary losses in the nephrotic syndrome, but these are rare causes of osteomalacia in patients on haemodialysis treatment. It is not clear to what extent defective production of calcitriol, characteristic of end-stage chronic renal failure is causally related to osteomalacia, in part due to uncertainties as to whether vitamin D acts directly on bone to promote mineralisation or whether its effects are mediated indirectly by modulating calcium and phosphate transport at other sites. Following the institution of renal replacement therapy, the incidence of osteomalacia varies markedly between renal units due to the skeletal retention of aluminium caused by the contamination of dialysis fluid or by the chronic ingestion of aluminium-containing phosphate binding agents. This form of osteomalacia is associated with a high risk of fracture, probably more related to depressed bone formation than to the presence of osteomalacia. Rarer causes of osteomalacia include parathyroidectomy and calcium and phosphate deficiency.
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PMID:Pathogenesis of osteomalacia in chronic renal failure and its relationship to vitamin D. 353 99

Previous reports have suggested that creatine kinase isoenzymes are elevated in patients with chronic renal failure and thus are less useful in the evaluation of chest pain in such patients. Our data in 88 patients with chronic renal failure receiving maintenance dialysis confirm this observation for total plasma creatine kinase. However, elevations in MB and BB creatine kinase, although statistically significant, were biologically unimpressive (5.9 +/- 0.05 [SEM] IU/L compared with 4.8 +/- 0.04 IU/L for MB creatine kinase [p less than 0.02], and 5.5 +/- 0.08 ng/ml compared with 3.2 +/- 0.05 ng/ml for BB creatine kinase [p less than 0.0002] ), and were unlikely to cause diagnostic confusion. In 92% of patients with chronic renal failure, plasma MB creatine kinase activity was within the normal range (less than 13 IU/L). Eight percent of patients manifested abnormal MB creatine kinase values; the highest was 20 IU/L. The glass bead method for measuring MB creatine kinase was used to avoid the potential confusion induced by non-creatine kinase-mediated fluorescence, which occurs in the region of MB and BB creatine kinase on electrophoresis. The infrequent and modest increases in plasma MB creatine kinase observed in patients with chronic renal failure should be appreciated, but it should not cause diagnostic confusion, because acute myocardial infarction usually results in more substantial elevations of MB creatine kinase.
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PMID:Unmasking artifactual increases in creatine kinase isoenzymes in patients with renal failure. 674 38

A 59-y-old with a history of chronic renal failure on hemodialysis was diagnosed with herpes zoster and begun on 800 mg acyclovir 5 times daily. Two days later the patient developed visual hallucinations, ataxia, confusion and memory loss along with focal myoclonus, nausea and vomiting. No fever, elevated WBC count or significant electrolyte imbalance was found. CT scan of the brain was unremarkable. The patient was then dialyzed for presumed acyclovir toxicity. Her acyclovir level was later found to have been 3.4 micrograms/ml (normal peak range 0.4-2 micrograms/ml) prior to dialysis. After 3 h of hemodialysis, her post-dialysis acyclovir level was 1.9 micrograms/ml. After a second course of hemodialysis the next day the patient's mental status improved, and she was discharged 5 d later. Due to its low volume of distribution (0.6 L/kg), low protein binding (about 15%) and water solubility, acyclovir is an example of the ideal drug that can be removed by hemodialysis. About 45% of the total body amount can be extracted through a 3-h course of hemodialysis with resultant improvement in symptoms.
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PMID:Hemodialysis removal of acyclovir. 757 52

A 25-year-old man developed nausea, vomiting, severe headache, and confusion. He had a past history of hyperuricemia and mild renal dysfunction. On admission he had somatic growth retardation, hypertrichosis, and bilateral auditory impairment. A cranial CT scan showed a small area of low density in the left temporal lobe and cerebellar atrophy. Five days later, he developed right homonymous hemianopia, sensory aphasia, and sensory inattention, and a new, large area of low density in the left occipital lobe on a cranial CT scan. On laboratory examination, lactate, pyruvate, and the lactate-to-pyruvate ratio were elevated in both the serum and cerebrospinal fluid. The biopsied muscle showed ragged red fibers and strongly SDH-reactive blood vessels. Gene analysis revealed the presence of the A 3243 G point mutation of the mitochondrial tRNA(Leu) gene in his blood leucocytes and muscle. Serum concentrations of BUN and creatinine were elevated to 46 mg/dl and 2.2 mg/dl, respectively. Creatinine clearance was 14.1 ml/min. An abdominal CT scan disclosed atrophy of his left kidney with subcapsular calcification and the findings of his abdominal ultrasonography were compatible with chronic renal failure. His mother, who suffered from renal failure and became dialysis dependent in her late forties also bore the A 3243 G mutation of the mitochondrial tRNA(Leu) gene in her circulating leucocytes. Though the association between MELAS and renal dysfunction still remains obscure, we speculate that renal failure can be a manifestation of MELAS.
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PMID:[Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with chronic renal failure: report of mother-child cases]. 897 30

Bilateral rupture of the quadriceps tendon is a rare injury. It usually occurs in obese older patients. Other predisposing factors are long-term chronic renal failure, gout, rheumatoid arthritis, diabetes mellitus, hyperparathyroidism and abuse of anabolic steroids. The most common cause of bilateral rupture is a sudden violent contraction of the quadriceps muscles with the knees semiflexed and the feet fixed. Examination reveals bilateral joint effusion, palpable or visible suprapatellar gaps, and an inability to extend both knees and lift the straight legs. Often the diagnosis is missed, and diagnostic confusion with other causes of inability to use the legs happens. We report one case of simultaneous bilateral rupture where treatment was delayed for several weeks because of diagnostic confusion.
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PMID:[Simultaneous bilateral rupture of the quadriceps tendon]. 962 90

Phenytoin toxicity is an uncommon problem seen in clinical practice. The predisposing factors for toxicity are hypoalbuminemia, chronic renal failure, hepatic dysfunction and drugs which interfere with phenytoin metabolism. Common manifestations of toxicity, like confusion and ataxia, are well known. A less well known phenomenon is paradoxical seizures. In this condition, seizures develop as the serum phenytoin level rises and decrease in frequency as levels drop. It may or may not be accompanied by other features of toxicity. We present three patients with paradoxical seizures; their serum phenytoin levels were 43.5 mcg/mL, 46.5 mcg/mL and 38.3 mcg/mL. In all cases, seizures were controlled by withdrawal of phenytoin and reduction of drug levels.
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PMID:Paradoxical seizures in phenytoin toxicity. 1048 84

The chemical composition of a dialysis membrane is decisive towards determining its physical and biochemical properties--two fundamental determinants of the success of therapy offered to patients suffering from chronic renal failure. From the vast variety of synthetic polymers available, only a few are suitable for the manufacture of dialysis membranes that have to conform to the diverse demands of modern haemodialysis and related therapies. Recently, a membrane labelled as polyamide (Polyamide S) has caused some confusion to end-users in that the product specification for the membrane is given as 'polyarylethersulfone' or simply as Polyamide S membrane. As the chemical and physical properties of these two polymer types are distinctly different, it is unclear whether the functional characteristics of Polyamide S are to be attributed to polyamide, polyarylethersulfone, or, to both polymers. We therefore undertook investigations to ascertain the exact chemical nature of the Polyamide S membrane using a series of chemical analytical tools and an appropriate polyamide reference. The analytical techniques were conventional gel permeation chromatography (GPC), GPC-FTIR coupled spectroscopy using dimethyl acetamide and hexafluoroisopropanol as solvents and nuclear magnetic resonance spectroscopy. Glass transition temperature measurements and quantitative elemental analysis were also carried out. None of the analytical techniques used showed any traces of polyamide in Polyamide S; no aliphatic or aromatic polyamide chemical entities were detected in any of the samples tested. The Polyamide S dialysis membrane thus comprises, solely, of polyarylethersulfone, which is also known as polyethersulfone.
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PMID:Verification of the chemical composition and specifications of haemodialysis membranes by NMR and GPC-FTIR-coupled spectroscopy. 1210 84

Non-convulsive status epilepticus related to cefepime has not been reported in childhood dialysis patients, although several adult cases have been reported. We report a state of acute confusion in a 15-year-old boy on continuous ambulatory peritoneal dialysis (CAPD) receiving cefepime that was diagnosed as status epilepticus by electroencephalography (EEG). The EEG improved after anticonvulsive therapy. All clinical symptoms disappeared dramatically within 24 h of discontinuation of cefepime. The differential diagnosis of confusional states and the mechanisms of the convulsive effects of antimicrobials in chronic renal failure are discussed. The importance that the clinician is aware of the rare side effects of antimicrobials is emphasized.
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PMID:Cefepime-induced non-convulsive status epilepticus in a peritoneal dialysis patient. 1498 79


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