Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study describes a spectrum of renal diseases that can precede the diagnosis of multiple myeloma (MM). Patients presenting manifestations of renal disease were recorded as individual patients of MM. Fifty patients (male 41; female 9) were included in this study. Diagnosis of MM was confirmed by two or more of the following four features: lytic bone lesions, serum or urine monoclonal peak, Bence Jones proteinuria, and greater than 20% plasma cells in bone marrow. Renal disease was present in 42 of 50 (84%) patients before MM was diagnosed. In only eight of 50 (16%) patients, diagnosis of MM preceded the detection of renal disease. Renal diseases consisted of acute renal failure in 26 patients (52%), chronic renal failure in 15 patients (30%) and nephrotic syndrome in 9 patients (18%). Some of the patients with acute or chronic renal failure also had heavy proteinuria. Percutaneous renal biopsy was done in 17 patients. Renal histopathology showed amyloidosis (n = 10), cast nephropathy (n = 5), nodular glomerulosclerosis (n = 1), and mesangioproliferative glomerulonephritis with plasma cell infiltration (n = 1). Hypercalcemia (calcium 11-13.8 mg/dL) was the most common precipitating factor for acute renal failure. All 50 patients received combination chemotherapy of melphalan and prednisolone or vincristine, Adriamycin, and dexamethasone. More than half of the total number of patients did not complete chemotherapy because of death or lost to follow-up. Nineteen patients with acute renal failure and eight patients with chronic renal failure were treated with hemodialysis. Fourteen patients (28%) with acute renal failure had recovery of renal function. Twenty-three patients (46%) were lost to follow-up. Seven patients (14%) died from sepsis, uremia, or hyperkalemia. Remission of MM was found in 9 of 21 (42.8%) patients who completed chemotherapy. Thus, acute renal failure is the most common renal disease preceding the diagnosis of MM. Reversal of renal function is achieved with chemotherapy and hemodialysis treatment.
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PMID:Renal disease is a prodrome of multiple myeloma: an analysis of 50 patients from eastern India. 1946 74

Unloading-induced atrophy is a relatively uncomplicated form of muscle loss, dependent almost solely on the loss of mechanical input, whereas in disease states associated with inflammation (cancer cachexia, AIDS, burns, sepsis, and uremia), there is a procatabolic hormonal and cytokine environment. It is therefore predictable that muscle loss mainly due to disuse alone would be governed by mechanisms somewhat differently from those in inflammatory states. We suggest that in vivo measurements made in human subjects using arterial-venous balance, tracer dilution, and tracer incorporation are dynamic and thus robust by comparison with static measurements of mRNA abundance and protein expression and/or phosphorylation in human muscle. In addition, measurements made with cultured cells or in animal models, all of which have often been used to infer alterations of protein turnover, appear to be different from results obtained in immobilized human muscle in vivo. In vivo measurements of human muscle protein turnover in disuse show that the primary variable that changes facilitating the loss of muscle mass is protein synthesis, which is reduced in both the postabsorptive and postprandial states; muscle proteolysis itself appears not to be elevated. The depressed postprandial protein synthetic response (a phenomenon we term "anabolic resistance") may even be accompanied by a diminished suppression of proteolysis. We therefore propose that most of the loss of muscle mass during disuse atrophy can be accounted for by a depression in the rate of protein synthesis. Thus the normal diurnal fasted-to-fed cycle of protein balance is disrupted and, by default, proteolysis becomes dominant but is not enhanced.
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PMID:Alterations of protein turnover underlying disuse atrophy in human skeletal muscle. 1960 31

This study was aimed at determining the median survival and most frequent causes of death in patients with the autosomal dominant polycystic kidney disease (ADPKD). A retrospective, observational analysis was made on patients registered with a diagnosis of ADPKD, in the computer records of the Sheffield Kidney Institute (SKI), United Kingdom, during the years 1981 to 1999. Data on 363 patients were analyzed from these computer records and further information, if any, was obtained from the patients' clinical notes. During this period, 88 patients died. The median age of the patients who died was 60.5 years, with the youngest being 37 years old and the oldest being 82 years. The major causes of death in this study group were cardiovascular (46.6%), infection (15.9%), central nervous system (CNS) disorders (11.36%), and miscellaneous causes (11.36%). Our study suggests that the major cause of death in patients with ADPKD was cardiovascular followed by infection, of which 42% of the deaths were due to septicemia. CNS causes of death comprised 11.36% of whom 60% had cerebrovascular events including subarachnoid hemorrhage in 20% of the patients. Uremia was the cause of death in only 2.2% of the patients in this series.
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PMID:Analysis of causes of mortality in patients with autosomal dominant polycystic kidney disease: a single center study. 1973 78

The prognostic of uremic syndrome had been improved by the development of renal replacement therapy. Uremic syndrome remains a dramatic medical concern in African sub-saharan countries. Nephrology practice has been introduced recently in Burkina Faso and epidemiological data on acute renal failure is not available. We conducted this study with the aim to describe the clinical profile of hospitalized patients. One hundred and twenty-one patients (18.4% of all admissions) with acute renal failure (creatinine>240micromol/L, abrupt onset) were included (age: 38.6+/-16.3y; creatinine: 1246.1+/-870.5micromol/L; urea: 40.2+/-18.3micromol/L), 75 men (age: 41.2+/-16.4) and 46 women (age: 34.2+/-15.2y). Acute renal failure was of medical cause in 91 cases, surgical cause in 16 cases and gyneco-obstetrical in 14 cases. Many pathophysiological factors have been identified like volume depletion, infections and obstruction. Acute renal failure was renal in 57 cases (age: 38.2+/-14.6y), prerenal in 43 cases (age: 36.8+/-16.7y) counting acute tubular necrosis in 21 cases, obstructive in 15 cases (age: 50.5+/-15.6y) and unclassified in six cases. Comorbidities have been identified: heart failure (13 cases), hepatocellular failure (eight cases), tumours (four cases) and severe hypertension (13 cases). Dialysis was justified in 84 cases but only accomplished in 14 cases. Hospital length of stay was 20.4+/-14.9 days. Twenty-nine patients died and causes were uraemia in 13 cases, hepatic in three cases, sepsis in 10 cases, malignant tumour in two cases and associated in one case.
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PMID:[Acute renal failure in Burkina Faso]. 1983 24

Growth hormone (GH) resistance is common in uremia and together with resistance to insulin-like growth factor-1 (IGF-1) contributes to uremic growth retardation and muscle wasting. Previously, we found decreased GH-stimulated janus-kinase 2-signal transducers and activators of transcription 5 (STAT5) phosphorylation and nuclear translocation in uremia; however, it is unclear whether there are more distal defects. Therefore, we tested whether the binding of phosphorylated STAT5b to DNA is intact in uremia. Using uremic rats we found that in addition to impaired hepatic STAT5b phosphorylation, the binding of available phospho-STAT5b to DNA is decreased thus contributing to impaired IGF-1 gene expression. As sepsis-induced inflammation causes a loss of body protein and as Gram-negative infections are relatively common in uremia, we also characterized mechanisms in which acute inflammation might contribute to GH resistance in uremia. Endotoxin-induced inflammation markedly increased the resistance to GH-mediated STAT5b signaling, and further decreased STAT5b binding to DNA and IGF-1 gene expression. These perturbations appear to be related to increased cytokine expression. Thus, our findings indicate that hepatic resistance to GH-induced IGF-1 expression in uremia arises due to defects in STAT5b phosphorylation and its impaired binding to DNA, processes further aggravated by inflammation.
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PMID:Uremia attenuates growth hormone-stimulated insulin-like growth factor-1 expression, a process worsened by inflammation. 2037 91

A functional ubiquitin proteasome pathway (UPP) is vital for all eukaryotic cellular systems and therefore any alteration in this critical component of proteostasis machinery has rpotential pathological consequences. A proteostasis imbalance can be induced by environmental pollutants, age or genetic factors. Though the exact underlying mechanisms are unclear, a decrease in proteasome activity weakens the homeostatic cellular capacity to remove proteins that are either misfolded or need to be replenished, which favors the development of neurodegenerative, cardiac and other conformational diseases. In contrast, induction of proteasome activity is an attribute of many diseases including muscle wasting, sepsis, cachexia and uraemia. In the case of misfolded protein disorders, higher degradation of a single protein leads to the pathophysiological consequences due to the absence of functional protein. Therefore, selective proteostasis inhibition is a potential treatment strategy for misfolded protein disorders, while broad-spectrum proteasome inhibitor drugs are designed to target tumor metastasis. In contrast, for muscle wasting and neurodegeneration, the use of proteostasis-activating or modulating compounds could be more effective.
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PMID:The case for therapeutic proteostasis modulators. 2125 Aug 74

Sepsis is a clinical syndrome related to severe infection and is characterized by systemic inflammation and injury to multiple organs and functional systems. Sepsis is one of the main causes of acute renal failure (ARF). Diuretics are frequently administered during ARF. However, there is scant evidence that diuretics provide any benefit to the patients with ARF. This case report highlights the occurrence of uremia and nonrecovery of renal function after administration of diuretics in a patient with ARF caused by sepsis. It is suggested that physicians should be cautious in prescribing diuretics to patients with ARF due to septicemia. Diuretics cause uremia and may lead to false diagnosis of chronic renal failure and nonrecovery of renal function. The patient may unnecessarily require prolonged dialysis.
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PMID:Diuretics induced uremia and nonrecovery of renal function in a patient with acute renal failure caused by sepsis. 2202 11

Anticoagulation of the extracorporeal circuit, necessary for the correct management of renal replacement treatment in acute renal failure, is essential. There is a high risk of bleeding secondary to the presence of complex platelet and coagulation abnormalities, the effect of uremia, recent surgery or a state of sepsis. This requires careful evaluation of the type of anticoagulation to be used to prevent blood clotting of the circuit, maintain filter efficiency, and minimize the risk of bleeding. In critically ill patients with no risk of bleeding, heparin is still the anticoagulant treatment of choice. With an increased bleeding risk or in particular situations such as HIT-II, dermatan sulfate can be safely used as an alternative to dilution driven. A valid additional resource in case of a high risk of bleeding is citrate, the use of which - thanks to its effectiveness and ease of use - is becoming more widespread. Citrate is able to provide regional anticoagulation without any interference with the patient. This makes it increasingly feasible to continue replacement therapy, allowing a sufficient number of hours to obtain the correct dialysis dose in critically ill patients with acute renal failure.
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PMID:[Citrate: an additional resource for anticoagulation in continuous replacement therapy]. 2238 3

Factor V Leiden, is a variant of human factor V (FV), also known as proaccelerin, which leads to a hypercoagulable state. Along these years, factor V Leiden (FVL) has been studied from the pathophysiologic point of view, and research has been focused on finding clinical approaches for the management of the FVL associated to a trombophilic state. Less attention has been paid about the possible role of FVL in inflammatory conditions known to be present in different disorders such as uremia, cirrhosis, liver transplantation, depression as well as sepsis, infection or, inflammatory bowel disease (IBD). Whether platelet FVL will increase the activation of coagulation and/or in which proportion is able to determine the final outcome in the previously mentioned inflammatory conditions is a subject that remains uncertain. This paper will review the association of FVL with inflammation. Specifically, it will analyze the important role of the endothelium and the contribution of other inflammatory components involved at both the immune and vascular levels. This paper will also try to emphasize the importance of being a FVL carrier in associations to diseases where a chronic inflammation occurs, and how this condition may be determinant in the progression and outcome of a specific clinic situation.
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PMID:Factor v leiden and inflammation. 2266 76

Ultrasound-guided cannulation of a large-bore catheter into the internal jugular vein was performed to provide temporary hemodialysis vascular access for uremia in a 65-yr-old woman with acute renal failure and sepsis superimposed on chronic renal failure. Despite the absence of any clinical evidence such as bleeding or hematoma during the procedure, a chest x-ray and computed tomographic angiogram of the neck showed that the catheter had inadvertently been inserted into the subclavian artery. Without immediately removing the catheter and applying manual external compression, the arterial misplacement of the hemodialysis catheter was successfully managed by open surgical repair. The present case suggests that attention needs to be paid to preventing iatrogenic arterial cannulation during central vein catheterization with a large-bore catheter and to the management of its potentially devastating complications, since central vein catheterization is frequently performed by nephrologists as a common clinical procedure to provide temporary hemodialysis vascular access.
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PMID:Unintended cannulation of the subclavian artery in a 65-year-old-female for temporary hemodialysis vascular access: management and prevention. 2309 28


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