ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00760.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00761.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00762.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

SummaryPotassium homeostasis is remarkably well preserved in the majority of patients on dialysis, despite the loss of the normal major route of potassium elimination. Nonetheless, the new major pathways for potassium removal (dialysis and gastrointestinal) are clearly less able to adapt to changes in potassium intake than is the healthy kidney. Therefore, disturbances in the plasma potassium concentration, most commonly hyperkalemia, remain a constant threat to the health of dialysis patients. A recent survey of outpatients on chronic hemodialysis found about a 10% incidence of severe predialysis hyperkalemia (serum potassium concentration greater than 6.0 mmol/L). Several causes of this potentially lethal problem must be considered when it occurs (Table 2). We hope that through a sound understanding of potassium homeostasis, the incidence of such serious disturbances in plasma potassium concentration can be reduced.

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00763.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

SummaryThe joint diseases that are encountered in chronic dialysis have been reviewed. There are two general categories: de novo disease and arthropathy anteceding ESRD. The de novo joint diseases include categories that are probably the direct result of ESRD. Microcrystalline CaOHapatite and CaPPD arthritis is associated with hyperparathyroidism and a high Ca X P. Aluminum phosphate joint disease is the result of aluminum toxicity. Both types have severe disease of the adjacent bone: osteitis fibrosa with CaOHapatite‐CaPPD arthropathy and osteomalacia with aluminum phosphate. Calcium oxalate joint disease probably results from renal oxalate retention in ESRD and conversion of ascorbate to oxalate. The evidence for uric acid arthropathy in the absence of primary gout or lead toxicity is not convincing. Amyloid is the most frequent cause of the carpal tunnel syndrome and is related to retention of β‐2 microglobulin. Infective arthritis may be Seen, often occumng as a result of bacteremia from an infected fistula site. A degenerative arthritis different from osteoarthritis has also been described. Pathologic fractures can occur with both amyloid deposition in bone and aluminum osteomalacia. Long‐term steroid therapy can lead to avascular necrosis of femoral or humeral heads. Diabetes mellitus with neuropathy can give rise to a very destructive Charcot joint. Tendon ruptures occur, but the mechanism is obscure.It is most important that the nephrologist work closely with the rheumatologist. Carefbl and sophis ticated examination of synovial fluid and tissue is mandatory in the microcrystalling diseases. Immunohistochemical methods may be required, particularly for tissue removed during decompression of the median nerve. Together the subspecialists can establish the diagnosis and determine the appropriate therapy for the iarge number of joint disorders to which the dialysis patient is s

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00764.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

SummaryLittle is actually known about the minimum daily requirement for most vitamins in the patient with end‐stage renal disease. Many of the studies reviewed suffer from lack of adequate control populations and differing methodologies, making comparisons between these studies difficult. However, patients with renal failure have many restrictions on their dietary intake, frequently suffer from intercurrent illness, and would seem to be at risk for vitamin deficiency. Also, metabolic abnormalities associated with the loss of kidney function may increase the daily requirements for certain vitamins. It is unlikely that dialysis losses of the water‐soluble vitamins alone could account for vitamin depletion, and these other factors are likely to play a much more important role.It is of interest to note that the studies which demonstrate little or no vitamin deficiencies are those studies which have been carried out more recently (8, 9, 17). The patients were usually given some vitamin supplementation prior to or during the period of study and thus it is not surprising that most patients failed to demonstrate vitamin deficiency. It is also likely that heightened awareness regarding the propensity for patients with renal failure to develop deficiencies of the water‐soluble vitamins has resulted in better dietary instruction and earlier intervention with vitamin supplementation. More efficient dialytic methods have also reduced the restrictions on many foods, and patients are no longer instructed to boil all their fresh vegetables. Although there may be the risk of toxicity when vitamin supplementation is overzealously administered to patients with reduced renal excretory function, it seems prudent to administer some of these water‐soluble vitamins to patients with end‐stage renal disease who are treated with intermittent dialysis therapy (Table 1). Certainly, this is not a very costly approach. Further studies should be carried out to better evaluate vitamin nutriture in chronically uremic and maintenance dialysis patients and to more rigorously define the minimum dose that would prevent deficiency and avoid

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00765.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

SummaryIt is clear that much research continues in an attempt to better understand DAH. A reasonable synthesis scenario based on current knowledge is as follows. Within the first 5–10 minutes of dialysis with a cellulosic membrane, blood contact leads to complement activation, generation of anaphylatoxins, leukoagglutination, and pulmonary microleukoaggregates. In addition, release of thromboxane in the lung occurs and causes pulmonary hypertension. This series of events causes mild hypoxemia and is preventable when noncellulosic membranes are used. As dialysis proceeds subsequent hypoxemia is dependent on the dialysate composition. With acetate dialysate, outward CO2dialysance occurs concomitant with inward acetate dialysance. This leads to reflex hypoventilation, increased oxygen consumption (which lowers RQ), and possibly direct central respiratory suppression. These changes account for the late hypoxemia seen. With bicarbonate dialysate, the above events do not occur. If rapid alkalinization ensues, however, because of a high dialysate bicarbonate concentration, hypoventilation and hypoxemia may be seen.A clear understanding of these pathophysiologic mechanisms provides a framework from which the preventative measures outlined can be understood and applied. Future research should focus on a better understanding of the sequence of events following blood‐membrane interaction, particularly in regard to activation of prostenoids. In addition, a more precise method is needed to determine the appropriate bath bicarbonate concentration for individual patients to avoid rapid alkalinization and hypoxemia. Finally, methods of identification of patients at risk of serious consequences from DAH need to be developed as well as noninvasive means of monitoring such individuals during dialysis. Much progress has been made in these areas in the past 10 years, but there is still more to le

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00766.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00767.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00768.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

ISSN:0894-0959    

DOI:10.1111/j.1525-139X.1988.tb00769.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY