Cyclosporine-induced changes in glomerular filtration rate and urea excretion

Laskow, David A.; Curtis, John J.; Luke, Robert G.; Julian, Bruce A.; Jones, Patsy; Deierhoi, Mark H.; Barber, William H.; Diethelm, Arnold G.

doi:10.1016/0002-9343(90)90429-h

Cited by 50 publications

(16 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The latter also responds less well than azathioprine-treated pa- tients to a converting enzyme inhibitor. 61 An effect of cyclosporine to enhance proximal tubular reabsorption of filtrate is supported by acute studies in humans showing diminished C H 2o/GFR during water diuresis, 63 enhanced urea absorption rates at the same urinary flow rates in cyclosporine-treated as compared with azathioprine-treated and hypertensive renal allograft recipients, 64 and an increased prevalence of hyperuricemia and gout in cyclosporine-treated patients. 65 Renal conservation of sodium in cyclosporine-treated patients is enhanced and excretion of a salt load diminished.…”

Section: Cyclosporine-induced Hypertension As a Modelmentioning

confidence: 97%

Essential hypertension: a renal disease? A review and update of the evidence.

Luke

1993

Hypertension

View full text Add to dashboard Cite

Section: Cyclosporine-induced Hypertension As a Modelmentioning

confidence: 97%

Essential hypertension: a renal disease? A review and update of the evidence.

Luke

1993

Hypertension

View full text Add to dashboard Cite

“…Many of the side effects of the CNIs surrounding CNI nephrotoxicity stem from the time when CsA was in early development and later with TAC use. CNIs induce vasoconstriction of the afferent arteriole by causing an imbalance between vasoconstrictor agents such as endothelin, thromboxane and activation of the renin-angiotensin system and decrease of vasodilator factors like prostaglandin E 2 , prostacyclin, and nitric oxide [14,15,16,17,18,19]. The arteriolar vasoconstriction induces an acute reversible impairment of renal function and also acute reversible tubular dysfunction.…”

Section: Acute Versus Chronic Cni Nephrotoxicitymentioning

confidence: 99%

Calcineurin Inhibitor Nephrotoxicity: A Review and Perspective of the Evidence

2013

View full text Add to dashboard Cite

Background: There is no doubt that acute calcineurin inhibitor (CNI) nephrotoxicity exists; however, chronic CNI nephrotoxicity is questionable at best. Methods: We reviewed the literature to identify original articles related to the use of CNIs in renal and nonrenal solid organ transplantation in order to examine the available evidence about their chronic nephrotoxicity and contribution to graft failure. Results: Early clinical experience and animal studies support the evidence of CNI nephrotoxicity. These findings evolved into the dogma that CNI nephrotoxicity is the major cause of late renal allograft failure. However, in transplanted kidneys the specific role of chronic CNI nephrotoxicity has been questioned. The emerging literature clearly highlights the lack of solid evidence for the role of CNIs as the sole and major injurious agents that cause chronic renal dysfunction and subsequent graft failure. Most of the evidence available to date is against complete CNI avoidance, and minimization appears to be a more viable strategy. It is becoming increasingly clear that the typical pathological lesions linked to chronic CNI use are highly nonspecific, and most of the chronic changes that have been attributed to chronic CNI nephrotoxicity are the consequences of previously unrecognized immunologic injuries. One needs to keep in mind that the potential risk of side effects of CNI use should be balanced against the risk of rejection. Conclusions: More research should focus on addressing the true causes of chronic graft dysfunction rather than focusing on the overexaggerated contribution of CNIs to late graft loss.

show abstract

“…Data using impaired renal function as the marker can result in a wider range of estimates because some impairment is expected for all patients who are on CNI therapy (17). Single-center data also can pro- vide useful insights into immunosuppressive regimens (cyclosporine versus tacrolimus), renal function pretransplantation, proteinuria measurements, and native-kidney biopsy status.…”

Section: Discussionmentioning

confidence: 99%

Increasing Referral for Renal Transplant Evaluation in Recipients of Nonrenal Solid-Organ Transplants

Chandrakantan

Mattos

Naftel

et al. 2006

Clinical Journal of the American Society of Nephrology

Self Cite

View full text Add to dashboard Cite

The use of cyclosporine and tacrolimus therapy in nonrenal (heart, heart/lung, lung, and liver) transplantation has resulted in improved patient and graft survival. Nephrotoxicity is one of the major side effects of tacrolimus and cyclosporine therapy and may lead to ESRD. The trend of referral of nonrenal solid-organ transplant recipients for kidney transplant evaluation at a large multiorgan transplant center was examined. Records of all patients who were referred for renal transplantation at the University of Alabama between January 1, 1993, and June 30, 2004, were reviewed. Eighty (0.96%) of 8318 individuals had previously undergone a nonrenal solid-organ transplant and were included in the study. The majority (72%) of patients had their nonrenal transplants performed at the University of Alabama. Twenty-two patients had their nonrenal transplant performed elsewhere and had fewer data available for analysis. From the period 1993-1996 to 2001-2004, an 11-fold increase in the absolute number of referrals of patients with nonrenal transplants was noted. Of patients who were referred for transplant evaluation, 25 became recipients of kidney transplants with a predominance of living-donor transplants. Referral for kidney transplant evaluation among nonrenal solid-organ transplant recipients is increasing and will exacerbate the existing shortage of deceased-donor kidneys that are available for transplantation. There was a trend for liver transplant recipients compared with other solid-organ recipients to develop ESRD at a greater rate.

show abstract

Cyclosporine-induced changes in glomerular filtration rate and urea excretion

Cited by 50 publications

References 21 publications

Essential hypertension: a renal disease? A review and update of the evidence.

Essential hypertension: a renal disease? A review and update of the evidence.

Calcineurin Inhibitor Nephrotoxicity: A Review and Perspective of the Evidence

Increasing Referral for Renal Transplant Evaluation in Recipients of Nonrenal Solid-Organ Transplants

Contact Info

Product

Resources

About