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)

Rhabdomyolysis is characterized by local or generalized skeletal muscle necrosis. It is caused by many clinical conditions and drug or alcohol abuse. Clinical symptoms are muscle pain and muscle weakness. Laboratory investigations show a rise in serum creatine phosphokinase and electrolyte disturbances. The most serious complication is acute renal failure. We present a patient with rhabdomyolysis and renal failure associated with a recent Influenza A virus infection.
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PMID:Rhabdomyolysis associated with influenza A virus infection. 776 Sep 69

Among the 153 patients fulfilling NINDS criteria for Guillain Barre' Syndrome (GBS) seen over 5.5 yrs, there were 47 (M:F 38.9) critically ill patients (age range 4 to 60 years). Antecedent event was recorded in 25 patients and the peak deficit was attained over a mean period of 9.5 days. Besides severe motor paralysis other salient features were: bulbar paralysis--42, sensory symptoms or signs--21, dysautonomia 31 and requirement for ventilatory assistance 45. CSF protein was raised in 63% cases. All the 17 patients who underwent electromyography had abnormalities of nerve conduction paramentes. Mean stay on the ventilator was 29.6 days and was not influenced by corticosteroid. Complications were frequent: pulmonary and urinary tract infection, dysautonomia, electrolyte disturbances, haemetmesis, bleeding from tracheostomy site and hepatic and renal failure. Mortality in steroids treated group (13/27) and the conservatively managed group (5/20) did not differ significantly. No discriminant factor emerged between survivors and non-survivors. Age and sex of the patients, presence of antecedent event, onset to peak interval and CSF protein level did not predict the need for ventilatory assistance, although these patients at admission had more frequent weakness of facial, bulbar, trunk, neck and proximal muscles of upper limbs and autonomic disturbances. Course of GBS remains unpredictable at the onset of the disease, warrants close supervision and meticulous supportive care and remains a therapeutic challenge.
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PMID:Critically ill Guillain Barre' syndrome. 786 87

We report a 78-year old woman with 30 years history of rheumatoid arthritis and nephrotic syndrome, who developed right hemiparesis and renal failure recently. The patient was diagnosed as having rheumatoid arthritis in 1965, and had been treated with gold -sol, steroid hormone, and non-steroidal anti-inflammatory drugs intermittently. Later on her clinical course was complicated by nephrotic syndrome, however, her renal function was well compensated. Otherwise, she was apparently doing well until October of 1988 when she had an onset of anomic aphasia; she was 73-year-old at that time. She was admitted to our hospital; a cranial CT scan at that time revealed a low density area in the left temporal region, and she was diagnosed as suffered from an atherothrombotic infarction involving the left middle cerebral artery territory. She recovered soon and was discharged for out patient follow up with ticlopidine 100 mg/day. She was doing well until December 15, 1990, when she had an acute onset of nausea, vomiting, and speech disturbance; she was admitted to our hospital for the second time. On admission, she was alert, but she had motor aphasia, right hemiparesis, and dysarthria. A cranial CT scan revealed a low density area in the left temporal region extending into adjacent frontal and parietal areas including the angular gyrus; in addition, leukoaraiosis, cortical atrophy, and ventricular dilatation were noted (Fig. 1A, B). She was treated supportively, and she showed improvement in her aphasia, however, moderate weakness remained in her right upper and lower extremities. She was discharged for out patient follow up. She was doing well until May 21, 1993, when she developed difficulty in swallowing and speech. She became unable to take foods orally and she was admitted again on May 31. On admission, she was afebrile and BP was 120/80 mmHg. General physical examination was unremarkable except for pitting edema and multiple contracture of her joints. On neurologic examination, she was alert but appeared to have aphasia and dementia; she could utter only a few simple words, and was able to understand only simple questions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 78-year-old woman with rheumatoid arthritis, right hemiparesis, and renal failure]. 789 38

The authors present a case report of a 62-year old woman, with hypertension for many years. She suffered from weakness, anorexia and weight loss in the last 6 months. On admission, anemia, elevated ESR, haematuria, proteinuria and renal failure were present. Renal biopsy was compatible with chronic glomerulonephritis. The clinical picture and positivity for P-ANCA suggested systemic vasculitis. Later evidence of maxillary sinusitis and nasal mucosae ulcers as well as pneumonitis, although biopsy did not reveal granulomas, suggested the diagnosis of Wegener Vasculitis. Medicated with Cyclophosphamide and Prednisolone, for a year, with improvement. The authors make a brief discussion of the clinical criteria for classification of ANCA-associated systemic vasculitis.
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PMID:[Vasculitis associated with ANCA]. 794 37

A 44-year old female was admitted to our hospital for evaluation of uncontrolled hypertension. She received renal transplantation 3 months ago and suffered from a tingling sensation and weakness on both hands. Laboratory findings (low serum potassium, low plasma renin activity and elevated plasma aldosterone level) was consistent with primary aldosteronism. Through the postural study for plasma aldosterone and the adrenal CT finding we diagnosed this case as adrenal adenoma, which was confirmed by surgical removal. A retrospective review of medical records showed that characteristic findings in primary aldosteronism (hypokalemia and low plasma renin activity) were masked by renal failure and became evident after successful renal transplantation. It was suggested that impaired urinary potassium excretion and excess release of renin from the ischemic kidney masked the characteristic findings of primary aldosteronism. To our knowledge, this is the first report documenting the change of renin-angiotensin-aldosterone system after renal transplantation in a case of coexistence of primary aldosteronism and chronic renal failure.
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PMID:Primary aldosteronism detected after renal transplantation. 797 85

Renal tubular acidosis (RTA) is a defect in urinary acidification in the absence of renal failure. All records of patients admitted to adult medical wards at the University Hospital USM (HUSM), Kelantan between 1986 to 1990 with the diagnosis of renal tubular acidosis were reviewed. Sixteen (16) patients were identified and fulfilled the diagnostic criteria. Their mean age at presentation was 28.9 +/- 0.74 years. The triad of muscle weakness, hypokalaemia and systemic metabolic acidosis were the characteristic features at presentation. Normal serum alkaline phosphatase and skeletal X-rays were noted. Their prognosis were generally good. Their mean serum bicarbonate and potassium on follow up were 17.84 +/- 0.35 and 3.82 +/- 0.05 mmol/L respectively. The importance of regular follow-up and long-term management is emphasised.
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PMID:Renal tubular acidosis in Kelantan, Malaysia--a case review. 799 10

Disorders in purine and pyrimidine metabolism may be difficult to recognize because their recent description means many are little known. They cover a broad spectrum of illnesses, can present from birth to the 80s, have multiple symptoms and lead to early death. Recognition of new disorders requires skill and serendipity. Often parents of affected children provide valuable clues. These disorders should be suspected, particularly where the history involves siblings, in anaemia, susceptibility to infection, or neurological deficits including autism, delayed development, epilepsy, self-mutilation, muscle weakness and - unusual in children and adolescents - gout. Some patients present with kidney stones, renal failure, alone or with the above, or as an intolerance/sensitivity to therapy (fluorouracil or azathioprine immunosuppression). These disorders can be detected from the abnormal metabolites in body fluids and/or altered enzyme activity. Abnormal cellular nucleotides or renal clearance may sometimes provide the only clue. Diagnosis can be difficult because of genetic heterogeneity and interference by blood transfusion, diet or drugs. Tests incorporating enzyme peak shifts and online diode-array detection are essential. Collaborative research is needed to improve the diagnosis and understanding of the metabolic basis for these sometimes devastating disorders and to apply this knowledge to the more common killers of mankind.
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PMID:When and how does one search for inborn errors of purine and pyrimidine metabolism? 803 39

We developed a mouse model of acute encephalopathy induced by verotoxin 2 variant (VT2v)-producing Escherichia coli. Three-week-old mice were inoculated intragastrically with approximately 10(10) CFU of E. coli O157:H- strain E32511/HSC and simultaneously given an intraperitoneal injection of mitomycin (MMC; 2.5 mg/kg). Drinking water containing 5 g of streptomycin sulfate per liter was given ad libitum from 3 days before the infection. From 1 to 2 days after bacterial inoculation, clinical features including weight loss, weakness, and flaccid paralysis of the extremities developed, usually culminating in death within 4 days. Diarrhea was not observed during the course of disease. No mice died in the absence of streptomycin or MMC treatment for 2 weeks after the oral bacterial infection. Judging from the clinical course and the biochemical and histological examination, the cause of death was not likely to be attributable to renal failure or to a side effect of MMC. To better understand the cause of death, we examined the brain cortex and spinal cord of the moribund mice by electron microscopy. Mice showing mortal symptoms were given horseradish peroxidase intravenously. The tracer was present in the endothelial basal lamina, in the surrounding extracellular spaces, and even in the neuron fibers of the brain cortex. Furthermore, immunoreactivity of VT2v, proved by the use of rabbit anti-VT2 serum, was localized selectively in the damaged myelin sheaths of neuron fibers which were accompanied by edematous axons in the brain cortex and spinal cord. These findings strongly suggest that VT2v is toxic to both endothelial cells and neurons in the central nervous system and subsequently causes fatal acute encephalopathy.
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PMID:Direct evidence of neuron impairment by oral infection with verotoxin-producing Escherichia coli O157:H- in mitomycin-treated mice. 803 16

A dog being treated with meglumine antimonate for leishmaniasis was examined because of anorexia, vomiting, diarrhea, weakness, and signs of abdominal discomfort. The history, physical examination findings, clinicopathologic abnormalities, and results of coagulation testing were compatible with a diagnosis of renal failure and disseminated intravascular coagulation. The signs of abdominal pain were most likely a result of microcirculatory obstruction. The cause of disseminated intravascular coagulation in this dog was not determined; however, visceral leishmaniasis could have been associated.
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PMID:Visceral leishmaniasis and disseminated intravascular coagulation in a dog. 804 4

A 38-year-old male presented to the emergent department complaining of bilateral leg numbness and weakness after waking from a sleep. Finding himself on the floor, he attributed this problem to falling out of bed. His subsequent course was complicated by progressive leg swelling, shock, profound hemoconcentration and renal failure. He received large volume of crystalloid and fasciotomy in the emergent department and then admitted. He ultimately recovered well. Crush syndrome without obvious compressive trauma or substance induced sleep is highly unusual. Early recognition is important because a delay of more than 6 hours in giving adequate volume support will lead to renal failure. Ischemic muscle times of greater than eight hours inevitably lead to residual disability. It remains imperative therefore, to recognize the presence of a compartment syndrome secondary to fluid sequestration early, either clinically or using compartment pressures. A fasciotomy within this eight hour window may still lead to complete recovery.
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PMID:Crush syndrome--delayed diagnosis due to a lack of apparent injury mechanism--a case report. 806 45


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