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)

Acute tumor lysis syndrome (ATLS), a condition which results from a rapid destruction of tumor cells with massive release of cellular breakdown products, has been well described following the treatment of various malignancies. However, only a handful of cases of spontaneous ATLS have been reported in the literature. We describe the first reported case of spontaneous ATLS in acute myeloid leukemia (AML). A previously healthy 63 year old woman presented with a two month history of fatigue and a one week history of easy bruising. On admission she had oliguric acute renal failure, with marked elevation in serum uric acid and phosphate. A bone marrow biopsy showed AML M7 with fibrosis. The renal failure resolved with supportive care and institution of allopurinol therapy. Following this, AML induction chemotherapy resulted in complete remission. Her biochemical and clinical course were very similar to the classical ATLS seen in patients after chemotherapy. Therefore, this case represents a rare instance of acute renal failure from spontaneous ATLS, and in our opinion the first reported occurrence of spontaneous ATLS associated with AML.
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PMID:Spontaneous acute tumor lysis syndrome in acute myeloid leukemia? A single case report with discussion of the literature. 964 77

A 47-year-old woman was admitted to our hospital for evaluation of general fatigue and dyspnea. She had been diagnosed with progressive systemic sclerosis (PSS) when she was 39 years of age, on the basis of Raynaud's phenomenon, proximal sclerosis, and pigmentation of the skin. On admission, her blood pressure was 206/128 mmHg. Funduscopy revealed grade III (Keith & Wagener) hypertensive retinopathy. Laboratory data showed positivity for anti-nuclear antibody and anticardiolipin beta 2 glycoprotein I antibody, and the plasma level of renin activity (PRA) was abnormally high. Chest X-ray and UCG revealed massive pericardial effusion. On the second hospital day, she was operated on for pericardiodiaphragmatic fenestration. The volume of pericardial effusion amounted to more than 2000 ml. Post operative malignant hypertension persisted. Laboratory data showed thrombocytopenia, hemolytic anemia, and acute renal failure. We diagnosed scleroderma renal crisis (SRC) associated with antiphospholipid syndrome. Following the initiation of angiotensin converting enzyme inhibitor (ACE-I) combined with calcium antagonist and alpha-one blocker, her blood pressure and PRA decreased. She also had been treated with aspirin 81 mg daily. These therapies were effective in recovering the platelet count and stopped the progression of anemia and renal failure. Although either the finding of large pericardial effusion or SRC is associated with poor prognosis in PSS, this case has had a good clinical course. In this case, the findings suggested that anti-phospholipid antibody may have contributed to the pericarditis and SRC.
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PMID:[A case of scleroderma renal crisis with massive pericardial effusion and positivity on antiphospholipid antibody test]. 965 14

Interest in measuring the quality of life (QL) in relation to health care has increased enormously in recent years. This is also true for end-stage renal failure where it is important not only to provide a better survival but also the quality of that survival. The aim of this study was to assess the relative influence of different kinds of treatment on end-stage renal disease after the patients' evaluation of their overall QL. We studied 167 patients receiving conservative treatment (45), haemodialysis (44), haemodialysis and erythropoieth (36), and continuous ambulatory peritoneal dialysis (42). The patients completed an original questionnaire consisting of 37 questions divided in five groups and generating 15 QL variables: personal data (name, gender, age, basic kidney disease); sociodemographic data influenced by the illness (family history, working ability, employment status); general health characteristics (fatigue, appetite, wound healing, sleep, resistance to cold); aspects of private life that are mostly influenced by the disease (social interaction, traveling, mood, sports, sexual life), and patients subjective assessment of their condition (self care and happiness). Patients on haemodialysis showed lower levels of QL than that on peritoneal dialysis related to fatigue (p < 0.01), working ability (p < 0.05), wound healing (p < 0.05), and appetite (p < 0.01) compared to the conservative treatment. Peritoneal dialysis had also a statistically significant positive influence on fatigue (p < 0.05) compared to conservative treatment. However, erythropoletin treatment showed better results with regard to traveling (p < 0.05), resistance to cold (p < 0.01), self care (p < 0.05) and mood (p < 0.05) compared to peritoneal dialysis, and working ability (p < 0.05), fatigue (p < 0.05) and mood (p < 0.05) compared to conservative treatment and haemodialysis.
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PMID:[Effect of various methods of treatment in chronic renal insufficiency on the quality of life in patients]. 986 10

Massive bee envenomation can produce both immediate and delayed toxic reaction. Signs and symptoms of immediate toxic reaction are fatigue, nausea, vomiting, hemolysis, kidney failure, and disseminated intravascular coagulation. The label "delayed toxic reaction" refers to a patient who is asymptomatic after a massive bee envenomation, with normal initial laboratory results, but later demonstrates laboratory evidence of hemolysis, coagulopathy, thrombocytopenia, rhabdomyolysis, liver dysfunction, and disseminated intravascular coagulation. The subject of this case report, a 66-year-old man, was stung more than 125 times in an attack by Africanized bees. He was initially asymptomatic, except for pain, and his laboratory findings were normal. The first signs of his fatal multi-organ-system failure were not apparent until 18 hours after envenomation. This experience has led the Good Samaritan Regional Poison Center in Phoenix, AZ, to recommend a 24-hour hospitalization for pediatric patients, older patients, and patients with underlying medical problems who are asymptomatic or who are experiencing only pain after an envenomation of 50 or more stings. Such patients have an increased risk of tissue injury, which may be delayed and which may be more effectively treated if identified early rather than on 12- to 24-hour follow-up. All other envenomated, asymptomatic patients or envenomated patients experiencing only pain who become symptomatic or who belatedly exhibit laboratory values consistent with hemolysis, thrombocytopenia, rhabdomyolysis, liver dysfunction, kidney failure, and disseminated intravascular coagulation within a 6-hour emergency department observation period should be admitted. Intravenous fluids, blood products, dialysis, and other intensive measures should be initiated if necessary.
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PMID:Delayed toxic reaction following massive bee envenomation. 1046 Jan 41

There is a high prevalence of protein-energy malnutrition in both nondialyzed patients with advanced chronic renal failure and in those individuals with end-stage renal disease who are receiving maintenance hemodialysis or chronic peritoneal dialysis therapy. Approximately one-third of maintenance dialysis patients have mild to moderate protein-energy malnutrition, and about 6 to 8 percent of these individuals have severe malnutrition. These statistics are of major concern because markers of protein-energy malnutrition are strong predictors of morbidity and mortality. The causes of protein-energy malnutrition in patients with chronic renal failure include: (1) decreased energy or protein intake; (2) concurrent chronic illnesses, and superimposed acute illnesses and possibly increased inflammatory cytokines; (3) the catabolic stimulus of hemodialysis; (4) losses of nutrients into dialysate, particularly amino acids, peptides, protein (with peritoneal dialysis), glucose (when hemodialysis is performed with glucose-free dialysate) and water-soluble vitamins; and (5) diagnostic or therapeutic (e.g., prednisone therapy) procedures that reduce nutrient intake or engender net protein breakdown. Other theoretically possible causes for protein-energy malnutrition include (6) chronic blood loss; (7) endocrine disorders (especially resistance to insulin and insulin-like growth factor-I, hyperglucagonemia, hyperparathyroidism and deficiency of 1,25-dihydroxycholecalciferol); (8) products of metabolism that accumulate in renal failure and may induce wasting, such as organic and inorganic acids; (9) loss of the metabolic actions of the kidney; and (10) the accumulation of toxic compounds that are taken up from the environment (e.g., aluminum).
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PMID:Pathophysiology of protein-energy wasting in chronic renal failure. 991 8

Cancer-related anaemia has a number of causes, not least the underlying malignancy itself which plays a role in suppressing erythropoiesis. Anaemia is often exacerbated by cancer treatments, in particular routinely used cytotoxic chemotherapy. Chronic anaemia of cancer is often characterized by inappropriately low levels of endogenous erythropoietin for the degree of anaemia, and manifests clinically with generalized hypoxia and resultant severe fatigue. Epoetin alfa is one recombinant form of erythropoietin, the primary human growth factor responsible for promoting proliferation and survival of erythroid progenitor cells. Epoetin alfa has been widely studied for the treatment of anaemia associated with renal failure and is now recognized as having significant potential in the management of cancer-related anaemia. Studies suggest that epoetin alfa is an effective treatment in a proportion of cancer patients with symptomatic anaemia. It also appears useful for the prevention of chemotherapy-induced anaemia. Studies in a number of different cancer settings have shown that epoetin alfa significantly increases haemoglobin and haematocrit, reduces transfusion requirements and improves quality of life for the patient.
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PMID:Epoetin in cancer-related anaemia. 1033 73

A 46-year-old female was admitted to our hospital due to general fatigue, systemic edema and dyspnea with history of systemic sclerosis (SSc). The patient was diagnosed as mixed connective tissue disease (MCTD) based on Raynaud phenomenon, a high anti-RNP antibody level and clinical symptoms and laboratory findings suggesting SSc, dermatomyositis (DM) and systemic lupus erythematosus (SLE). After the admission, both alveolar hemorrhage and a rapidly progressive glomerulonephritis (RPGN) also developed and laboratory findings showed a positive remark of myeloperoxydase-antineutrophil cytoplasmic antibody (MPO-ANCA) and anti-glomerular basement membrane (GBM) antibody. She was therefore re-diagnosed as microscopic polyarteritis nodosa (microscopic PAN) combined with MCTD and treatment with high dose prednisolone and steroid pulse therapy dramatically improved general conditions and lung symptoms, but maintenance dialysis was persistent because of irreversible renal failure. However, 3 months after the admission, she died of acute exacerbation of interstitial pneumonitis that was unresponsive to steroid pulse therapy. Autopsy revealed interstitial pneumonitis with alveolar hemorrhage and crescentic glomerulonephritis (CrGN), in which immunofluorescent microscopy showed no deposition in agreement with pauciimmune type. The histological findings supported the diagnosis; primary microscopic PAN combined with MCTD, which is a quite rare case, to our knowledge. Furthermore, co-existence of MPO ANCA and anti-GBM antibody, clinical and histological findings of the case also lead us to reconsider the relevance of these antibodies to pathogenesis and/or categories of microscopic PAN and Goodpasture's syndrome.
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PMID:[A case of mixed connective tissue disease with microscopic polyarteritis nodosa associated with perinuclear-antineutrophil cytoplasmic antibody and anti-glomerular basement membrane]. 1061 88

Simvastatin belongs to a class of lipid-lowering drugs which completely inhibit 3-hydroxy-3-methylglutaryl co-enzyme A (HMG CoA) reductase. The commonest adverse effects of therapy with simvastatin HMG CoA reductase inhibitors are gastro-intestinal disturbance, myositis and myopathy. Rhabdomyolysis leading to renal failure has been reported, but it appears to be very rare, except in patients also receiving cyclosporin, nicotinic acid or gemfibrozil. Here we report the case of an elderly lady who was known to have chronic renal failure, but who developed rhabdomyolysis following simvastatin therapy. Her symptoms of muscle pain, fatigue, myoglobulinuria, oliguria and pulmonary oedema appeared 48 h after the first dose of simvastatin. Simvastatin was immediately stopped, and the patient was dialysed for 1 week. Her renal function improved and came back. We suggest that extreme care should be exercised in prescribing this drug, particularly for the elderly with renal impairment.
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PMID:Simvastatin-induced rhabdomyolysis in a patient with chronic renal failure. 1127 41

We studied a case of a 63 year old Japanese man who presented in October, 1994 with general fatigue, low grade fever, micro hematuria and leukocytosis, elevated CRP as well as liver dysfunction. A liver biopsy at that time revealed mild cholangiolitis. Six months later he was admitted because of weight loss, protein urea, and renal failure. At that time he was positive for antineutrophil cytoplasmic antibody(ANCA) with perinuclear staining patter(p-ANCA) done by indirect immunofluorescence. He was also positive for anti-myeloperoxidase antibody(MPO-ANCA) done by ELISA. A renal biopsy showed idiopathic crescentic glomerulonephritis with pauci-immune type(ICGN). Despite therapy with steroids and cyclophosphamide, which improved his subjective symptoms, his renal failure accelerated necessitating hemodialysis which he has been on for over four years. In conclusion, this patient has a rare case of ICGN that presented with liver dysfunction similar to autoimmune hepatitis. Since ANCA has been known to be associated with systemic vasculitides as well as chronic inflammatory diseases(e.g. ICGN, microscopic polyarteritis nodosa, ulcerative colitis or autoimmune liver diseases), both the crescent formation in this patient's glomeruli and cholangiolitis in his liver may have shared the common etiology related to ANCA.
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PMID:[A case of ANCA positive idiopathic crescentic glomerulonephritis initiated with fever and liver dysfunction]. 1089 76

Primary (AL, amyloid light-chain) amyloidosis is a plasma cell disorder in which deposits of amyloid light-chain protein cause progressive organ failure. It is important to recognise that amyloidosis is a dynamic process and chemotherapy-induced reduction of the activity of the plasma cell clone reduces the supply of the amyloid precursor protein and can result in a major regression of the deposits. The most common target organ is the kidney and renal amyloidosis manifests as proteinuria or nephrotic syndrome. Proteinuria is seen in three quarters of patients. Amyloid related nephrotic syndrome and renal failure are potentially reversible. Fatigue, congestive heart failure, hepatomegaly, peripheral neuropathy, orthostatic hypotension, carpal tunnel syndrome and macroglossia are other common features. The median survival is one to two years. Conventional-dose melphalan as standard treatment can prolong the median duration of survival by about ten months, but the clinical response rates with improvement of impaired organ function are low. Up-front high-dose chemotherapy with autologous peripheral blood stem cell transplantation is much more effective and can result in a major improvement in the clinical condition of patients. However, the toxicity related to this treatment can be relevant due to impaired organ function. Conventional-dose chemotherapy consisting of vincristine, doxorubicin and dexamethasone or high-dose dexamethasone or interferon-alpha are other possible approaches to treatment. The improvement of patient condition with an effective conventional-dose chemotherapy may increase the tolerability of high-dose chemotherapy and reduce transplantation related problems.
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PMID:Novel approaches to the treatment of primary amyloidosis. 1106 Aug 11


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