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Renal disease interpretation

However, these data are limited and must be interpreted with caution, since NSAIDs have significant toxic effects on the kidney only in patients at risk (that is those with volume depletion, heart failure, cirrhosis, intrinsic renal disease, and hypercalcemia), in whom the secretion of vasodilator prostaglandins is increased in an attempt to counteract the effect of increased renal vasoconstrictors, such as angiotensin II. [Pg.1008]

Obstruction of the pancreatic duct by a calculus or by carcinoma of the pancreas may increase serum LPS activity depending on the location of the obstruction and the amount of remaining functioning tissue. In patients with a reduced glomerular filtration rate, the serum LPS activity is increased. Thus care should be exercised in the interpretation of elevated serum LPS values in the presence of renal disease. Finally, investigation of the biliary tract by endoscopic retrograde pancreatography or treatment with opiates (which causes the sphincter of Oddi to contract) may increase serum LPS activity. [Pg.621]

Interpretation Plasma osmolality should decrease by >5 mOsm/kg, and urine osmolality should drop to <100 mOsm/kg, with 90% or more of the water load excreted in 4 hours. SIADH is characterized by excretion of <90% of the water load and by urine osmolality that remains at >100mOsm/kg. Plasma ADH may be measured at 90 or 120 minutes after the water loading to confirm the diagnosis. Subnormal responses are seen with glucocorticoid deficiency, hypothyroidism, and renal diseases,... [Pg.1995]

In clinical chemistry, the variations of the Na concentration level in the extracellular fluid are interpreted as follows [3] (1) The level of Na" is elevated in dehydration (water deficit), central nervous system trauma or disease, and hyperadrenocorticism with hyperaldosteronism or corticosterone of corticosteroid excess. (2) A decrement of the Na level is observed in adrenal insufficiency, in renal insufficiency (especially with inadequate Na intake), in renal tubular acidosis as a physiological response to trauma and bums (Na shifts into cells), in unusual losses via the gastrointestinal tract as in acute or chronic diarrhea or intestinal obstruction or fistula, and in unusual sweating with inadequate sodium replacement. In some patients with edema associated with cardiac or renal disease, seram Na concentration is low, even though total body sodium content is greater than normal water retention (excess antidiuretic hormone, ADH) and abnormal distribution of sodium between intracellular and extracellular fluid contribute to this paradoxical situation. Hyperglycemia occasionally results in a shift of intracellular water to the extracellular... [Pg.572]

We have also noticed that hypertension, when it occurs in HGPRTase deficient subjects before middle age, is not an early feature, but is usually seen in people with severe gouty arthritis who already have evidence of renal disease and gouty arthritis (Observation 6). We interpret this as suggesting that hypertension may be a sequel to the formation of microtophi within the kidney. [Pg.158]

Comment Determination of RI is the most common measure giving information on renal perfusion and on vascular resistance. Several renal arteries must be checked for correct interpretation. RI is angle-independent, but influenced by factors such as heart rate, cardiac output, blood viscosity, and medications such as vasopressor support. Thus, pathologic values should be compared to values of other arteries to exclude systemic changes. A side difference of RI may indicate unilateral renal disease... [Pg.511]

The current values for ruling out a cardiac etiology for dyspnea are a BNP less than 100 pg/mL (100 ng/L) or an NT-proBNP less than 300 pg/mL (300 ng/L or 35.4 pmol/L). BNP measurements require cautious interpretation, as numerous conditions can also elevate BNP concentrations. These include older age, renal dysfunction, pulmonary embolism, and chronic pulmonary disease. Nesiritide, a recombinant BNP drug, has an identical structure to native BNP and will interfere with the commercial BNP assay, resulting in a falsely elevated level. Therefore, blood for BNP determination should be obtained 2 hours after the end of a nesiritide infusion, or alternatively the NT-proBNP assay should be utilized. [Pg.53]

There are several different kinds of laboratory safety data that require interpretation. These include routine screening for study subject selection, diagnostic evaluation of the subject, identification of risk factors, monitoring the progress of the disease or treatment, detection of adverse reactions, determination of appropriate dosages for certain at-risk subject groups (e.g. those with renal impairment). [Pg.263]

Renal/Hepatic function impairment- Because of an increased fraction of unbound phenytoin in patients with renal or hepatic disease, or in those with hypoalbuminemia, interpret total phenytoin plasma concentrations with caution. Unbound phenytoin concentrations may be more useful in these patients. After IV administration, fosphenytoin clearance to phenytoin may be increased without a similar increase in phenytoin clearance. This has the potential to increase the frequency and severity of adverse events. [Pg.1208]

The assessment of the nutritional state of renal patients has come under scrutiny in recent years. While serum albumin has served as the common index of nutritional status, evidence is mounting that interpretation of this parameter is influence by other factors. Recently, Ikizler et al. [159] provided evidence of an interaction between depleted nutritional status and active inflammatory disease as providing markers for increased risk of hospitalization for chronic hemodialysis patients. This awareness of the impact of inflammation on nutrition status requires further evaluation in order to properly assess the contribution of each to the progressive atherosclerotic disease, which characterized ESRD patients [160]. [Pg.18]

An association between the use of 5-ASA in patients with chronic inflammatory bowel disease and the development of a particular type of chronic tubulo-in-terstitial nephritis is difficult to interpret since renal involvement in chronic inflammatory bowel disease may be an extra-intestinal manifestation of the underlying disease [110]. Extra-intestinal manifestations of chronic inflammatory bowel disease are well recognized. The most frequent renal complications are oxalate stones and their consequences such as pyelonephritis, hydronephrosis and on the long-term amyloidosis [111, 112]. As for many drugs, reversible acute interstitial nephritis has been described [90]. [Pg.412]

Determination of PTH is useful in the differential diagnosis of both hypercalcemia and hypocalcemia for assessing parathyroid function in renal failure and for evaluating parathyroid function in bone and mineral disorders (see Calcium, Clinical Significance, Hypocalcemia, and Hypercalcemia Metabohc Bone Diseases and Interpretation of PTH Results). [Pg.1915]

ALB was one of the first identified biochemical markers of malnutrition and has long been used in population studies. ALB is a relatively insensitive index of early protein malnutrition because there is a large amount normally found in the body (4 to 5 g/kg of body weight), it is highly distributed in the extravascular compartment (60%), and it has a long half-life (18 to 20 days). However, chronic protein deficiency in the setting of adequate nonprotein calorie intake leads to marked hypoalbuminemia because of a net ALB loss from the intravascular and extravascular compartments (kwashiorkor). Serum ALB concentrations also are affected by moderate-to-severe calorie deficiency hepatic, renal, and GI disease and infection, tramna, stress, and burns. In many cases, interpretation of serum ALB concentrations relative to nutrition status is difficult however, a positive correlation between decreased serum ALB concentrations and poor clinical outcome has been demonstrated in a variety of settings. Additionally, serum ALB concentrations of 2.5 g/dL or less can be expected to exacerbate ascites and peripheral, pulmonary, and GI mucosal edema due to decreased colloid oncotic pressure. [Pg.2564]

An association between the use of 5-ASA in patients with chronic inflammatory bowel disease and the development of a particular type of chronic tubulointerstitial nephritis is difficult to interpret since renal involvement in chronic inflammatory bowel disease... [Pg.273]

Interpretation of Wilson s disease on the basis of disrupted copper metabolism is far from complete. The accumulation of copper in tissues is generally considered responsible for the lesions of the liver (cirrhosis), renal tubules (amino aciduria), and basal ganglia (neurological disorder), but the special affinity of these various tissues for copper remains to be explained, as does the mechanism of copper toxicity in these organs. Penicillamine, a copper-chelating substance, has been administered for treatment of Wilson s disease with some degree of success. In fact, it has even been claimed that asymptomatic victims of Wilson s disease can be treated preventively [56]. [Pg.163]


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See also in sourсe #XX -- [ Pg.52 ]




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Renal disease

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