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Kidney complicated

The high metabolic rate and work load of renal cells increases its susceptibility to toxicants. Furthermore, the kidney possesses biotransformation enzymes that can result in formahon of toxic metabolites and reactive intermediates which can damage renal macromolecules. Because the nephron has specialized transporters for reabsorption and excrehon, toxicants can enter and accumulate within renal cells, leading to nephrotoxicity. Finally, the unique functions of the varied segments along the nephron impart different susceptibilities to toxicants in the kidney, complicating the potential toxicities and subsequent renal damage via a variety of mechanisms. In this chapter, we will review some of these sites and mechanisms of nephrotoxicity. [Pg.73]

Blood plasma and ultrafiltrate concentrations of urea and creatinine have been studied with subcutaneous ultrafiltrate probes in diabetic dogs. The dogs had varying degrees of kidney complications secondary to the diabetes. [Pg.192]

Other etiologies for urinary tract dilatation include duplex kidneys complicated by a dilatation of the upper or the lower pole (Abuhamad et al. 1996 Vergani et al. 1999). Such anomalies can be associated with an ectopic extravesical ureter (Fig. 13.12) or an ectopic ureterocele (Fig. 13.13), which can be demonstrated in utero. [Pg.256]

The complex thioamide lolrestat (8) is an inhibitor of aldose reductase. This enzyme catalyzes the reduction of glucose to sorbitol. The enzyme is not very active, but in diabetic individuals where blood glucose levels can. spike to quite high levels in tissues where insulin is not required for glucose uptake (nerve, kidney, retina and lens) sorbitol is formed by the action of aldose reductase and contributes to diabetic complications very prominent among which are eye problems (diabetic retinopathy). Tolrestat is intended for oral administration to prevent this. One of its syntheses proceeds by conversion of 6-methoxy-5-(trifluoroniethyl)naphthalene-l-carboxyl-ic acid (6) to its acid chloride followed by carboxamide formation (7) with methyl N-methyl sarcosinate. Reaction of amide 7 with phosphorous pentasulfide produces the methyl ester thioamide which, on treatment with KOH, hydrolyzes to tolrestat (8) 2[. [Pg.56]

A common cause of PTH-dependent hypercalcemia results from benign, or occasionally malignant, enlargement of one or more parathyroid glands, a condition known as primary hyperparathyroidism (PHPT). Although many patients with PHPT present in an asymptomatic state that does not require medical intervention, some are afflicted with excess bone loss, kidney stones, or other complications. If patients are... [Pg.303]

Glucocorticoids increase the risk of gastrointestinal complications caused by NSAEDs. Considerable caution is necessary when using NSAIDs in patients with severe liver and kidney damage and they should not be combined with coumarines. Owing to the limited experience obtained, these precautions and contraindications also apply to COX-2-selective inhibitors. [Pg.874]

Diabetes mellitus is a complicated, chronic disorder characterized by either insufficient insulin production by the beta cells of die pancreas or by cellular resistance to insulin. Insulin insufficiency results in elevated blood glucose levels, or hyperglycemia As a result of the disease, individuals with diabetes are at greater risk for a number of disorders, including myocardial infarction, cerebrovascular accident (stroke), blindness, kidney disease, and lower limb amputations. [Pg.487]

Figure 20, Demonstration of disparity between nonprotein nitrogen and urea levels in a patient with terminal kidney disease complicated by liver involvement... Figure 20, Demonstration of disparity between nonprotein nitrogen and urea levels in a patient with terminal kidney disease complicated by liver involvement...
From a therapeutic point of view, it is essential to confirm the presence of bacteriuria (a condition in which there are bacteria in the urine) since symptoms alone are not a reliable method of documenting infection. This applies particularly to bladder infection where the symptoms of burning micturition (dysuria) and frequency can be associated with a variety of non-bacteriuric conditions. Patients with symptomatic bacteriuria should always be treated. However, the necessity to treat asymptomatic bacteriuric patients varies with age and the presence or absence of underlying urinary tract abnormalities. In the pre-school child it is essential to treat all urinary tract infections and maintain the urine in a sterile state so that normal kidney maturation can proceed. Likewise in pregnancy there is a risk of infection ascending from the bladder to involve the kidney. This is a serious complication and may result in premature labour. Other indications for treating asymptomatic bacteriuria include the presence of underlying renal abnormalities such as stones which may be associated with repeated infections caused by Proteus spp. [Pg.140]

The most common complication of CKD is anemia, which is caused by a decline in erythropoietin production by the kidneys and can lead to cardiovascular disease. [Pg.373]

Patients who progress to ESRD require renal replacement therapy (RRT). The modalities that are used for RRT are dialysis, including HD and peritoneal dialysis (PD), and kidney transplantation. The United States Renal Data Service (USRDS) reported that the number of patients with ESRD was 452,957, with 102,567 new cases being diagnosed in 2003.2 The most common form of RRT is dialysis, accounting for 72% of all patients with ESRD. The principles and complications associated with dialysis are discussed below. Chapter 52 discusses the principles of kidney transplantation. [Pg.394]

Bacteriuria, or bacteria in the urine, does not always represent infection. For this reason a number of quantitative diagnostic criteria have been created to identify the amount of bacteria in the urine that most likely represents true infection (hence the term significant bacteriuria ). These are shown in Table 76-1. Furthermore, UTIs are classified as lower tract or upper tract disease. Patients will present differently with upper versus lower tract disease, and upper tract disease is thought of as a much more severe infection, as patients are more likely to be admitted to the hospital with upper urinary tract disease than lower tract disease. An example of lower tract infection is cystitis. Cystitis refers to the syndrome associated with a UTI involving dysuria, frequency, urgency, and occasional suprapubic tenderness. An example of upper urinary tract disease is pyelonephritis. Pyelonephritis is an inflammation of the kidney usually due to infection. Frequently, patients with uncomplicated UTI are treated as outpatients, while those patients with complicated UTIs are treated as inpatients. [Pg.1151]

World-wide, about 130 million people are believed to suffer from diabetes, a disease which occurs when the body does not adequately produce the insulin needed to maintain a normal circulating blood glucose (80-120 mg/dl). It is estimated that the disease is in rapid expansion (300 million in 2025). Frequent monitoring of blood glucose is crucial for effective treatment and to reduce the morbidity and mortality of diabetes. Blindness, kidney and heart failure, peripheral neuropathy, pure circulation, gangrene are the severe complications which, over time, are related to diabetes. [Pg.429]

The isomerism existing between the pairs of nucleotides was attributed to the different locations of the phosphoryl residues in the carbohydrate part of the parent nucleoside,49 63 since, for instance, the isomeric adenylic acids are both hydrolyzed by acids to adenine, and by alkalis or kidney phosphatase to adenosine. Neither is identical with adenosine 5-phosphate since they are not deaminated by adenylic-acid deaminase,68 60 and are both more labile to acids than is muscle adenylic acid. An alternative explanation of the isomerism was put forward by Doherty.61 He was able, by a process of transglycosidation, to convert adenylic acids a" and 6 to benzyl D-riboside phosphates which were then hydrogenated to optically inactive ribitol phosphates. He concluded from this that both isomers are 3-phosphates and that the isomerism is due to different configurations at the anomeric position. This evidence is, however, open to the same criticism detailed above in connection with the work of Levene and coworkers. Further work has amply justified the original conclusion regarding the nature of the isomerism, since it has been found that, in all four cases, a and 6 isomers give rise to the same nucleoside on enzymic hydrolysis.62 62 63 It was therefore evident that the isomeric nucleotides are 2- and 3-phosphates, since they are demonstrably different from the known 5-phosphates. The decision as to which of the pair is the 2- and which the 3-phosphate proved to be a difficult one. The problem is complicated by the fact that the a and b" nucleotides are readily interconvertible.64,64... [Pg.296]

Vasopressin is a potent vasoconstrictor that increases blood pressure and systemic vascular resistance. It may have several advantages over epinephrine. First, the metabolic acidosis that frequently accompanies cardiopulmonary arrest can blunt the vasoconstrictive effect of epinephrine this does not occur with vasopressin. Second, stimulation of P receptors by epinephrine can increase myocardial oxygen demand and complicate the postresuscitative phase of CPR. Vasopressin can also have a beneficial effect on renal blood flow in the kidney, causing vasodilation and increased water reabsorption. [Pg.92]

Rare painless hematuria normal Hb level heavy exercise under extreme conditions may provoke gross hematuria and complications Pain crises, microvascular disruption of organs (spleen, liver, bone marrow, kidney, brain, and lung), gallstone, priapism, leg ulcers, anemia (Hb 7-10 g/dL) Painless hematuria and rare aseptic necrosis of bone vasoocclusive crises are less common and occur later in life other complications are ocular disease and pregnancy-related problems mild anemia (Hb 10-12 g/dL)... [Pg.385]

See Chap. 46, Chronic Kidney Disease Progression-Modifying Therapies, authored by Melanie S. Joy, Abhijit Kshirsagar, and Nora Franceschini, and Chap. 47, Chronic Kidney Disease Management of Complications, authored by Joanna Q. Hudson, for a more detailed discussion of this topic. [Pg.887]


See other pages where Kidney complicated is mentioned: [Pg.353]    [Pg.307]    [Pg.353]    [Pg.667]    [Pg.353]    [Pg.307]    [Pg.353]    [Pg.667]    [Pg.294]    [Pg.338]    [Pg.6]    [Pg.181]    [Pg.86]    [Pg.32]    [Pg.305]    [Pg.581]    [Pg.295]    [Pg.79]    [Pg.133]    [Pg.141]    [Pg.423]    [Pg.110]    [Pg.23]    [Pg.25]    [Pg.338]    [Pg.376]    [Pg.377]    [Pg.412]    [Pg.885]    [Pg.1146]    [Pg.1463]    [Pg.202]    [Pg.826]    [Pg.56]    [Pg.68]    [Pg.89]    [Pg.1727]    [Pg.877]   
See also in sourсe #XX -- [ Pg.204 , Pg.205 , Pg.247 ]




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Complicance

Complicating

Complications

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