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)

A 74-year-old housewife was admitted to the hospital with complaints of high fever and general fatigue. The physical examinations on admission showed no particular findings except for mild hepatomegaly, but laboratory findings showed severe liver dysfunction, active inflammation and negative tuberculine test. On the 4th day, she suddenly complained of severe respiratory distress. A chest X-ray film demonstrated surprising changes in comparison with that taken on admission. On suspicion of adult respiratory distress syndrome (ARDS) associated with military tuberculosis (Miliary TB), administration of Methylpredonisolone (1000 mg a day for 3 days) in addition to antituberculous drugs was immediately started. With this therapy she was recovered from such ill condition, but the general exhaustion and slight fever continued. We suspected that her condition might be due to adrenocortical involvement of Miliary TB and hormonal examinations were performed. Unexpectedly, Cushing's syndrome was suspected on the basis of the following; high level of plasma cortisol without normal daily variation, normal ACTH level, an absent response to the Dexamethasone suppression test. Computed tomography revealed left side adrenal mass. During these examinations, renal dysfunction probably due to Miliary TB grew gradually worse and she died of renal failure on the 56th day. Necropsy revealed disseminated tuberculosis involving the lungs and the liver, but the adrenal glands were not examined.
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PMID:[A case of miliary tuberculosis (miliary TB) accompanied with adult respiratory distress syndrome (ARDS) in a patient with Cushing's syndrome]. 140 68

Despite elevated parathyroid hormone (PTH) levels, low normal or diminished serum 1,25(OH)2D3 concentrations are found in patients with incipient renal failure. To further assess (indirectly) the reserve capacity of renal production of 1,25(OH)2D3 we studied 9 patients with incipient or moderate renal failure (inulin clearance 31-68ml/min/1.73 m2) and 9 controls, using a novel stimulation test. We measured 1,25 (OH)2D3 levels, free 1,25(OH)2D3 index, cAMP excretion, calciuria and phosphaturia before and after infusion of 2 x 400 U of human (h) PTH (1-38). Baseline 1,25(OH)2D3 levels were not significantly different in patients (42.5 pg/ml, 21.6-51.1) compared with controls (45.0 pg/ml, 37.4-67.3). After infusion of hPTH(1-38), however, median increase in 1,25(OH)2D3 was only +25% versus +86% in controls, despite a greater proportional increase in cAMP/GF ratio. The data suggest subnormal stimulation of renal 1,25(OH)2D3 production in response to exogenous PTH in most patients with incipient renal failure. This may reflect partial exhaustion of biosynthetic reserve capacity.
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PMID:Attenuated rise of 1,25 (OH)2 vitamin D3 in response to parathyroid hormone in patients with incipient renal failure. 201 72

Cardiac catheterisation was performed to evaluate cardiac function in 12 patients with various stages of renal failure. All patients were studied at rest and during supine exercise to subjective exhaustion. Eight patients had a normal arteriovenous oxygen difference at rest and during exercise whereas three had a low arteriovenous oxygen difference and one a high arteriovenous oxygen difference. Left ventricular stroke work did not increase normally at transition from rest to exercise in most patients with serum creatinine concentrations greater than 500 mumol/l. The left ventricular end diastolic pressure was abnormally raised during exercise in all patients (range 20-42 mm Hg) and also at rest in most of them (range 8-36 mm Hg), indicating myocardial dysfunction. These observations suggest that patients have abnormal cardiac performance at a relatively early stage of renal failure.
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PMID:Cardiac performance in various stages of renal failure. 650 67

An increase in the rate of lipid peroxidation and exhaustion of protective antioxidative factors were detected in blood of patients with chronic glomerulonephritis in renal failure. The severity of renal failure did not affect noticeably the alteration of the patterns studied, while the most serious impairments were found in patients with the nephrotic syndrome. The value of antioxidation coefficient whose calculation is given in the paper may be used as an integral pattern evaluating impartially the ratio between pro- and antioxidation factors. The drugs with antioxidative properties should be involved in routine courses of glomerulonephritis treatment especially in the nephrotic syndrome.
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PMID:[Features of lipid peroxidation in the blood of patients with chronic glomerulonephritis at the stage of renal dysfunction in the presence of nephrotic syndrome]. 833 80

Laboratory electrolyte and acid-base analyses are important for the characterization and assessment of the severity of disorders of fluid balance, and they enable the veterinarian to institute appropriate corrective therapeutic interventions. Abnormalities of electrolytes or acid-base rarely define the diagnosis, but certain diseases are characterized by predictable trends in these parameters. Important clinical situations in which assessment of electrolyte and acid-base status should be regarded as important to the equine practitioner include diarrhea, severe colic, peritonitis, pleuritis, dysphagia (inability to drink water or ingest food), neurologic dysfunction, exhaustion, renal failure, and rhabdomyolysis.
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PMID:Electrolyte and acid-base disturbances in the horse. 892 22

Many patients with solid tumours or haematological malignancies develop anaemia, and the use of chemotherapy aggravates this condition. Red blood cell transfusions are often necessary but are associated with many risks, including immunosuppressive effects that may increase the risk of tumour recurrence. Many clinical studies have shown that epoetin (recombinant human erythropoietin) therapy can ameliorate, or even prevent, the anaemia associated with chemotherapy and cancer (including solid tumours as well as multiple myeloma or lymphoma). Response, defined as a significant (>50%) reduction in the rate of transfusions and/or a significant (>2 g/dl) elevation of haemoglobin levels, is usually observed in about 60% of the patients, irrespective of the type of standard chemotherapy given. The decrease in transfusion requirements is the major objective of epoetin therapy, because they are costly, inconvenient and are associated with potential adverse effects. Epoetin therapy also brings about substantial improvements in various indices of quality of life that are proportional to changes in haemoglobin level. However, large dosages of epoetin are generally required and about 40% of patients do not respond even to very high dosages. A number of adverse effects of epoetin therapy have been observed in patients with renal failure. The most prominent include hypertension, headaches, seizures and thrombotic events. These complications can also occur in patients with renal failure who are not receiving epoetin. Their exact incidence has been assessed in placebo-controlled studies, which have demonstrated that there is no increased risk of thrombosis or seizure with epoetin. However, it is now generally accepted that 10 to 20% of haemodialysis patients will experience an elevation of blood pressure because of epoetin and there is no doubt that a rapid elevation of blood pressure may cause generalised seizures. In other settings, including anaemia associated with cancer, very few adverse effects have been attributed to epoetin. However, close monitoring of blood pressure should be implemented in patients with hypertension. There is no evidence that epoetin stimulates tumour growth. With the dosages of epoetin currently used, there is no evidence of stem cell competition, resulting in thrombocytopenia or neutropenia, or of stem cell exhaustion, producing secondary anaemia when treatment is stopped. Epoetin is a remarkably well tolerated drug that offers significant benefits in patients with cancer.
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PMID:A risk-benefit assessment of epoetin in the management of anaemia associated with cancer. 980 42

Ascites is the most frequent major complication of liver cirrhosis. Even if a significant decrease in renal clearances may be observed in the first stages of chronic active hepatitis, true renal impairment, often with the typical signs of hepatorenal syndrome, only occurs in patients with ascites, especially when tense and refractory. Experimental and clinical data suggest the presence of primary sodium and water retention, perhaps as a consequence of an increase in intrahepatic hydrostatic pressure. The abnormal sodium retention leads to plasma volume expansion, followed by decreased peripheral vascular resistances and increased cardiac output. This second stage concords with the peripheral arterial vasodilation theory, characterized by an increase in total blood volume, but with a decrease in effective arterial blood volume. This discrepancy leads to the activation of sympathetic nervous and renin-angiotensin-aldosterone systems. This activation, while protective against splanchnic and systemic vasodilation, provoked by the increased availability of nitric oxide and other vasodilating substances, induces renal vasoconstriction. This phenomenon can be considered as the basis of the progressive renal failure that leads to hepatorenal syndrome, favored by progressive exhaustion of the renal autacoid vasodilating substances. The first therapeutic approach to ascites is sequential and based on diuretic administration. Subsequently, paracentesis with albumin infusion is carried out, as well as transjugular intrahepatic portosystemic shunting, surgical portosystemic shunting, and liver transplantation: these procedures are essential for the treatment of hepatorenal syndrome.
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PMID:Pathogenetic factors and clinical elements in ascites and hepatorenal syndrome during liver cirrhosis. 1063 19

Ascites is the most common complication occurring during liver cirrhosis. Even if a significant decrease in renal clearance may be observed in the first step of chronic active liver disease, renal impairment, at times complicated by the typical signs of hepatorenal syndrome, occurs only in patients with ascites, especially when tense and refractory. Experimental and clinical data seem to suggest a primary sodium and water retention in the pathogenesis of ascites, in the presence of an intrahepatic increase of hydrostatic pressure, which, by itself, physiologically occurs during digestion. Abnormal sodium and water handling leads to plasma volume expansion, followed by decreased peripheral vascular resistance and increased cardiac output. This second step is in agreement with the peripheral arterial vasodilation hypothesis, depicted by an increase in total blood volume, but with a decreased effective arterial blood volume. This discrepancy leads to the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems associated with the progressive activation of the renal autacoid systems, especially, that of the arachidonic acid. During advanced cirrhosis, renal impairment becomes more sustained and renal autacoid vasodilating substances are less available, possibly due to a progressive exhaustion of these systems. At the same time ascites becomes refractory inasmuch as it is no longer responsive to diuretic treatment. Various pathogenetic mechanisms leading to refractory ascites are mentioned. Finally, several treatment approaches to overcome the reduced effectiveness of diuretic therapy are cited. Paracentesis, together with simultaneous administration of human albumin or other plasma expanders is the main common approach to treat refractory ascites and to avoid a further decrease in renal failure. Other effective tools are: administration of terlipressin together with albumin, implantation of the Le Veen shunt, surgical porto-systemic shunting or transjugular intrahepatic portosystemic stent-shunt, or orthotopic liver transplantation, according to the conditions of the individual patient.
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PMID:Update on ascites and hepatorenal syndrome. 1250 17

The organotypic stem cell of skeletal muscle has previously been known as satellite cell. They allow muscle fiber growth during ontogenesis, enable fiber hypertrophy and are responsible for the very efficient repair of muscle fibers. This efficient apparatus is to some degree counterbalanced by an enormous use of the satellite cell pool: fiber atrophy probably is accompanied by loss of myonuclei such that every reversal of atrophy is bound to use new myonuclei i.e. satellite cells. How often in life does this occur? Hard to say. Moreover, the potent repair capacity is challenged by an unexpected vulnerability of skeletal muscle fibers: Passive stretching of contracted muscles may cause multiple "microdamage," disruption of contractile elements or tiny areas of true necrosis (focal necrosis). How often does this happen? Well, for many of us at least once per year when we go up and down mountains during vacation time, followed by sour muscles. Others may decide to change his/her (locomotor) behaviour by severe onset of jogging; it may happen that they suffer kidney failure on Monday due to muscle microdamage and the transfer of myoproteins into the serum over weekend. Also 20 minutes of stepping up and down something like a chair will do: There is a remarkable increase in kreatin kinase and other muscle derived proteins which lasts for days and is bound to reflect some muscle damage. How about sportsmen and worker who repeatedly use their muscles in such a way? We don't have answers yet to most of these questions, but considerable amount of information has been collected over the last years both in animal and--less--in human. What is common in all cases of growth and repair is the proliferation of the satellite cells and their consequent incorporation and fusion with the parent fiber. This way focal damage is repaired often without visible reminders. We would run out of satellite cells were they not stem cells: After division one daughter remains a satellite cell while the other is free to divide. Divide how often? Important for the human cells since the cell ages and proliferates slower and slower till it stops to divide at all, at least in culture. The same is true for the new satellite cell. This we know from recent experiments in which human biopsies derived myogenic cells were grown in vitro and in vivo (by implanting them into skeletal muscles of immunoincompetent mice): Growth correlates negatively with age of the donor. Between age 2 and some 70 years, about two divisions are performed by each satellite cell in human vastus lateralis and biceps brachii muscle in 10 years in the average. Most important for the older among us: at age 76 there are still some 13 divisions left before complete exhaustion. However, there are diseases like Duchenne Muscular Dystrophy (DMD) in which muscle fibers lack a structural protein with the effect of enhanced vulnerability to mechanical stress. There the enhanced use of the satellite cell pool makes the remaining growth capacity in an 8-years-old child as low as otherwise found at age 80. Some time ago, implantation of genetically intact myoblasts obtained from healthy relatives has been proposed as a treatment of DMD. Every logic would have predicted that some local implantation of whatever numbers of cells was bound to fail rescue the complete masculature or at least the muscles for breathing. The human as guinea pig? Now, even years later, we still collect the basic information on growth of human myoblasts and start thinking of ways for systemic application and quantitatively relevant incorporation of the myogenic stem cell or other--possibly pluripotent--stem cells derived from bone marrow.
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PMID:[Regeneration capacity of skeletal muscle]. 1295 31

We report a 20-year-old male who suffered smoke inhalation injury and burns covering 26% of his TBSA, including his face, dorsal chest, and both the arms. The Abbreviated Burn Severity Index was 5 (likelihood of survival 95%). He underwent burn surgery, requiring massive transfusion. Postoperatively, he appeared increasingly hyperthermic, showed respiratory exhaustion, and was neutropenic (lowest white blood cell count was 0.8 Gpt with a normal granulocyte count). He developed acute respiratory distress syndrome, renal failure, and severe inflammatory response syndrome. Aggressive ventilation patterns, intermittent prone positioning, and high-dose catecholamine therapy were performed. Hydrocortisone therapy and antibiotic prophylaxis did not improve his clinical status. He died after 12 days of septic multiple organ failure. Legal medicine autopsy identified aggressive Candida famata mycosis. The organism mainly affected the alimentary canal, and there were multiple pyemic abscesses in tissues of the heart, liver, spleen, kidneys, lungs, and meninges. Histology confirmed gastric ulcers as the source of the Candida infection. Despite the autopsy findings, all intravital specimens collected (blood, urine, and tracheal mucus) and all clinical Candida antigen tests were unsuspicious. Postoperative neutropenia may be a warning sign of severe infection even in survivable burns. Suppression of immune response and possible previous gastric Candida colonization may contribute to hazardous outcomes. However, delayed and unreliable methods to detect fungal infections remain a major problem in burn care. Occult aggressive fungal sepsis resulting in early multiple organ failure should be kept in mind.
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PMID:Fulminant, undetected Candida sepsis after an apparently survivable burn injury. 1969 26


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