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Acquired renal disease

Eremina, V, Sood, M, Flaigh, J. Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseases. J Clin Invest, 111 707-l 6, 2003. [Pg.534]

End-slage renal disease is defined as the situation where the GFR falls below 20 ml/min (Martin, 1996). Each year, over 30,000 persons in the United States acquire end-stage renal disease. Hypertension is the most common complication of end-... [Pg.477]

Aweeka FT, Jacobson MA, Martin-Munley S, Hedman A, Schoenfeld P, Omachi R, Tsunoda S, Gambertogho JG. Effect of renal disease and hemodialysis on foscamet pharmacokinetics and dosing recommendations. J Acquir Immune Defic Syndr Hum Retrovirol 1999 20(4) 350-7. [Pg.1448]

A cystic renal cell carcinoma and acquired renal cystic disease associated with consumption of chaparral tea has been reported (7). [Pg.3733]

Smith AY, Feddersen RM, Gardner KD Jr, Davis CJ Jr. Cystic renal cell carcinoma and acquired renal cystic disease associated with consumption of chaparral tea a case report. J Urol 1994 152(6 Pt 1) 2089-91. [Pg.3733]

RaoTK, Friedman EA, Nicastri AD.The types of renal disease in the acquired immunodeficiency syndrome. N Engl J Med 1987 316 1062-1068. [Pg.612]

Combinations of poor dietary supply, intestinal malabsorption because of the antagonistic effects of other trace elements, or blockage of uptake by substances Uke phytate — together with increased excretory losses as a result of disease, injury, and infection—can result in overt, symptomatic trace element deficiency disease. Liver disease, inflammatory bowel disease, and renal disease will affect trace element absorption and excretion to a variable extent and may cause an acquired deficiency disease. [Pg.1119]

Nephrogenic Diabetes Insipidus. Failure of the kidney to respond to normal or increased concentrations of AVP can cause NDI. In the majority of these patients, AVP is mcapable of stimulating cychc adenosine monophosphate (cAMP) formation. Two causes have been described for this disorder (1) mutation in the vasopressin receptor and (2) mutations in the aquaporin-2 water channels. Hie vasopressin receptor mutation form of NDI is an X-chromosome-linked disorder that mostly affects males. Females are more likely to have the aquaporin-2 water channel gene defect on chromosome 12,ql2-13, which produces an autosomal recessive disease. Acquired forms of NDI may be caused by metabolic disorders (hypokalemia, hypercalcemia, and amyloidosis), drugs (hthium, demeclocycline, and barbiturates), and renal diseases (polycystic disease and chronic renal failure). NDI may also be seen in the absence of these factors (idiopathic). [Pg.1992]

Polycythemia is characterized by an increase in the number, and in the hemoglobin content, of circulating red cells. In patients who have chronic anoxia from impaired pulmonary ventilation or congenital or acquired heart disease, the increase in plasma erythropoietin leads to secondary polycythemia. Some renal cell carcinomas, hepatocarcinomas, and other tumors, which produce physiologically inappropriate amounts of erythropoietin, may also cause secondary polycythemia. Conversely, anemia can result from renal insufficiency and from chronic disorders that depress erythropoietin production. In polycythemia vera (primary polycythemia), which is a malignancy of erythrocyte stem cells of unknown cause, erythropoietin levels are normal or depressed. [Pg.657]

Healthy individuals require 10 to 30 milliunits/mL of EPO to maintain normal Hgb and Hct concentrations. Endogenous EPO levels can increase 100- to 1,000-fold during hypoxia or anemia. This marked increase does not occur in patients with end-stage renal disease, patients receiving chemotherapy, and patients with acquired immunodeficiency syndrome (AIDS), especially those taking azidothymidine. These patients will have an EPO response that is insufficient to correct their anemia. [Pg.1813]

In this condition the renal tubules are unresponsive to antidiuretic hormone and, as such, the subject has polyuria. The condition may be congenital or acquired. Acquired nephrogenic diabetes insipidus can result from several causes, such as chronic renal disease, potassium deficiency including primary aldosteronism, drugs such as lithium, systemic diseases such as multiple myeloma, and chronic hypercalcemias, including hyperparathyroidism. The damage to the renal tubules... [Pg.142]

Gout is a metabolic disease characterized by recurrent episodes of acute arthritis, usually monoarticular, and is associated with abnormal levels of uric acid in the body, particularly the presence of monosodium urate crystals in synovial fluid. Primary gout is a hereditary disease in which hyperuricemia is caused by an error in uric acid metabolism—either overproduction or an inability to excrete uric acid. Secondary gout refers to those cases in which hyperuricemia is caused by an acquired disease or disorder, such as chronic renal disease, lead poisoning, or myeloproliferative disorders. Gout generally occurs in... [Pg.1436]

The failure of vascular access (VA) represents the major cause of morbidity for those end-stage renal disease patients on hemodialysis, and access maintenance is the most frequent cause of hospitalization for such patients [1]. The subsequent extended length of stay commonly encountered in older patients is also related to further adverse events as hospital-acquired infections and fever, prolonged catheterization predisposing to central venous obstruction and delay in access revision with increased associated costs. The VA maintenance cost increases 5-fold for those patients with a failed autogenous access [2]. [Pg.165]

Simple and acquired renal cysts are rare in infancy and childhood. US usually detects them as an incidental finding. Possible manifestation of a polycystic or dysplastic renal disease must be considered necessitating at least regular follow-up and nephro-urologic check-up. [Pg.203]

Levine E (1992) Renal cell carcinoma in uremic acquired renal cystic disease incidence, detection and management. Urol Radiol 13 203-210... [Pg.209]

Hogg RJ (1992) Acquired renal cystic disease in children prior to the start of dialysis. Pediatr Nephrol 6 176-178 Hogg RJ, Furth S, Lemley KV et al (2003) National Kidney Foundation s kidney outcomes quality initiative clinical practice guidelines for chronic kidney disease in children and adolescents Evaluation, classification, and stratification. Pediatrics 111 1416-1421... [Pg.412]

Lerner GR, Warady BA, Sullivan EK et al (1999) Chronic dialysis in children and adolescents. The 1996 Annual Report of the North American Pediatric Renal Transplant Cooperative Study. Pediatr Nephrol 13 404-417 Levine E (1992) Renal cell carcinoma in uremic acquired renal cystic disease incidence, detection, and management. Urol Radiol 13 203-210... [Pg.412]

Merck (2003) Principles of transplantation suppression of the immune system (2003) www.merck.com/mmhe/ print/secl6/chl87/chl87b.html Miller L, Soffer O, Nannan V (1989) Acquired renal cystic kidney disease in end stage renal disease an autopsy study of 155 cases. Am J Nephrol 9 322-328 Oniscu G, Brown H, Forsythe J (2004) How old is old for transplantation Am J Transplant 4 2067-2074 Pessione F, Cohen S, Durand D, Hourmant M, Kessler M, Legendre C (2003) multivariate analysis of donor risk fac-... [Pg.9]


See other pages where Acquired renal disease is mentioned: [Pg.613]    [Pg.400]    [Pg.362]    [Pg.401]    [Pg.422]    [Pg.613]    [Pg.400]    [Pg.362]    [Pg.401]    [Pg.422]    [Pg.135]    [Pg.139]    [Pg.191]    [Pg.135]    [Pg.603]    [Pg.743]    [Pg.1952]    [Pg.391]    [Pg.399]    [Pg.253]    [Pg.187]    [Pg.191]    [Pg.193]    [Pg.207]    [Pg.358]    [Pg.404]    [Pg.407]    [Pg.412]    [Pg.73]    [Pg.88]    [Pg.270]   
See also in sourсe #XX -- [ Pg.362 , Pg.401 , Pg.422 ]




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Acquired

Renal disease

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