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This section introduces the rationale for developing a definition of chronic kidney disease and classification of stages of severity; risk factors for adverse outcomes of chronic kidney disease; the relationship between disease severity and rate of progression as risks for adverse outcomes; the definitions and stages defined by the Work Group; and laboratory tests for the detection of each stage. More reliable estimates of the prevalence of earlier stages of disease and of the population at increased risk for development of chronic kidney disease; 2. Recommendations for laboratory testing to detect earlier stages and progression to later stages; 3. Evaluation of factors associated with a high risk of progression from one stage to the next or of development of other adverse outcomes; 5. Clinical practice guidelines,clinical performance measures,and continuous quality improvement efforts could then be directed to stages of chronic kidney disease. Defining chronic kidney disease and stages of severity requires ‘‘categorization’’ of continuous measures of markers of kidney damage and level of kidney function. Identify ing the stage of chronic kidney disease in an individual is not a substitute for diagnosis of the type of kidney disease or the accurate assessment of the level of kidney function in that individual. However,recognition of the stage of chronic kidney disease would facilitate application of guidelines,performance measures,and quality improvement ef forts. In other fields of medicine,classifications of stages of severity of illness have been adopted with apparent success,such as the New York Heart Association classification of heart disease. Within nephrology and related disciplines,classifications of disease severity have been developed that are based on ‘‘categorization’’ of continuous measures of disease severity. For example,the Joint National Committee for the Prevention,Detec tion,Evaluation and Treatment of High Blood Pressure has defined stages of hypertension based on blood pressure level. The National Cholesterol Education Program has defined stages of hypercholesterolemia based on serum cholesterol level. These classifications have facilitated epidemiologi cal studies,clinical trials,and application of clinical practice guidelines. Risk Factors for Adverse Outcomes of Chronic Kidney Disease A risk factor is defined as an attribute that is associated with increased risk of an outcome. This guideline concerns itself primarily with identifying susceptibility and initiation factors to define individuals at high risk of developing chronic kidney disease,and with progression factors,to define individuals at high risk of worsening kidney damage and subsequent loss of kidney function. Relationship Between Disease Severity and Rate of Progression as Risks for Adverse Outcomes In principle,one may distinguish between the severity of disease and the risk for adverse outcomes of disease. The severity of disease can be determined from measurements of level of organ function,complications in other organ systems,morbidity (symptoms and clinical findings),and impairment in overall function and well-being. In addition,the risk for adverse outcomes is also dependent on the rate of progression to a more severe stage or the rate of regression to a less severe stage. For the case of chronic kidney disease,these concepts can be illustrated by Fig 4.
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The diagnostic and prognostic value of amniotic fluid white blood cell count, glucose, interleukin-6 and Gram stain in patients with preterm labor and intact membranes. A comparative study of the diagnostic performance of amniotic fluid glucose, white blood cell count, interleukin-6, and Gram stain in the detection of microbial invasion in patients with preterm premature rupture of membranes. Romero R, Sibai B, Caritis S, Paul R, Depp R, Rosen M, Klebanoff M, Sabo V, Evans J, Thom E, Cefalo R, McNellis D. Antibiotic treatment of preterm labor with intact membranes: A multicenter, randomized, double-blinded, placebo-controlled trial. Interleukin-1 and tumor necrosis factor stimulate arachidonic acid release and phospholipid metabolism in human myometrial cells. P h y s i o l o g y : Electromechanical activities of human uteri during extra-corporeal perfusion with ovarian steroids. Prevention of preeclampsia with low-dose aspirin in healthy, nulliparous pregnant women. The National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units. Neutrophil attractant/activating peptide-1/interleukin-8: Association with histologic chorioamnionitis, preterm delivery, and bioactive amniotic fluid leukoattractants. Prenatal diagnosis of fetal cutaneous hemangioma: A case report and review of the literature. Relationship between the fetal biophysical profile score, umbilical artery Doppler velocimetry, and fetal blood acid-base status determined by cordocentesis. Prenatal diagnosis of spontaneous rupture of the fetal bladder using color Doppler ultrasonography. Topographic differences in amniotic fluid concentrations of prostanoids in women in spontaneous labor at term. Brief report: Umbilical cord ligation of an acardiac twin by fetoscopy at 19 weeks of gestation. The biomolecular mechanisms of preterm labor in women with intrauterine infection. Tumor necrosis factor-α in pregnancies associated with preeclampsia or small-for-gestational-age newborns. Systemic and local cytokine profiles in endotoxin-induced preterm parturition in mice. Macrophage inflammatory protein-1α in term and preterm parturition: Effect of microbial invasion of the amniotic cavity. The value of amniotic fluid interleukin-6, white blood cell count, and Gram stain in the diagnosis of microbial invasion of the amniotic cavity in patients at term. The natural interleukin-1 receptor antagonist in the fetal, maternal, and amniotic fluid compartments: the effect of gestational age, fetal gender, and intrauterine infection. Ultrasonographic examination of the uterine cervix is better than cervical digital examination a s a p r e d i c t o r o f t h e l i k e l i h o o d o f p r e m a t u r e d e l i v e r y in patients with preterm labor and intact membranes.
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Furthermore, phosphorus is also required for protein and hydrolysis of triglycerides provides necessary structural incorporation into phospholipids, nucleopro precursors for hepatic gluconeogenesis, which provide a teins and nucleic acids. There is also incorporation of source of glucose for hematologic and neurologic cells. During prolonged starvation, there are additional mech Hypokalemia anisms to produce glucose and conserve substrates. This yields less attributed to the reintroduction of carbohydrate and the Copyright © Lippincott Williams & Wilkins. There is typically a (a) diaphragm fatigue, whole-body reduction of potassium during starvation, (b) respiratory failure, and which accentuates the problems of hypokalemia during (c) prolonged ventilatory weaning. Depletion of magnesium during the refeeding process is (6) Immunologic: multifactorial. As with phosphorus and potassium, there (a) immune suppression, and is a total body depletion of magnesium during starvation. Serum levels may be deceptively normal due to concur (7) Neurologic: rent dehydration. Weakness Hyperglycemia Muscular weakness is commonly seen in the refeeding Upon reintroduction of carbohydrate to a patient experi syndrome. Thisweaknesscanbesynergisticwithweakness encing starvation, gluconeogensis is initially suppressed. It is mainly However, as refeeding continues, glucocorticoid circula driven by electrolyte aberrations, primarily hypophospate tion increases leading to exacerbation of hyperglycemia. Sodium retention and uid imbalance Arrhythmia the hyperinsulinemic response to carbohydrate in the Both hypomagnesaemia and hypokalemia are associated starved patient causes decreased renal excretion of with cardiac arrhythmias . The retention of sodium and water as potentially lethal ventricular arrhythmias [36,37]. This enzyme is required for ef?cient of?oading Vitamin and mineral de?ciencies may already be present of oxygen to peripheral tissues. As a result, even in the in a patient experiencing starvation from prolonged presence of normal gas exchange, delivery of oxygen to inadequate intake . Limited thiamine Cardiac dysfunction stores can be utilized early in the refeeding process. The introduction of adequate nutrition places signi?cant metabolic stress on marginalized myocardium. The already poorly functioning heart may be unable to handle Clinical implications the additional volume from the uid retention associated There are a number of clinical consequences to the with the refeeding syndrome [7,39,40]. Most of these are the result of tion represented the causes of death among prisoners in electrolyte shifts and vitamin depletion. The characteristics of the refeeding syndrome are as follows: Respiratory failure Hypophosphatemia is a well known mediator of diaphrag (1) Electrolyte abnormalities: matic fatigue. The refeeding syndrome can lead to new (a) hypokalemia, respiratory failure or prolonged ventilator weaning [8,23]. The (3) Cardiac: remaining thiamine is used up very rapidly after the (a) heart failure, and introduction of a glucose source.
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