Acute Hyperuricemic Nephropathy and Renal Failure after Transplantation

Venkataseshan, V S; Feingold, Robert M; Dikman, Steven; Churg, Jacob

doi:10.1159/000186160

Cited by 11 publications

(7 citation statements)

References 8 publications

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“…Evidence that hyperuricemia causes or contributes to progressive kidney disease or CVD is weak, even in the general population (804,818,819). Acute kidney injury from very high uric acid levels has been reported (820). A large registry cohort study recently demonstrated an association of gout with elevated mortality (adjusted hazard ratio 1.26, 95% CI 1.08–1.47) and graft loss (adjusted hazard ratio 1.22, 95% CI 1.01–1.49) (808).…”

Section: Rationalementioning

confidence: 99%

Special Issue: KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients

Eckardt¹,

Kasiske²,

Zeier³

2009

American Journal of Transplantation

1,205

294

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Journal compilation © 2009 The American Society of Transplantation and the American Society of Transplant Surgeons doi: 10.1111/j.1600-6143.2009.02834.x S2 American Journal of Transplantation 2009; 9 (Suppl 3): S2-S2Since the first successful kidney transplantation in 1954 It is our hope that this document will serve several useful purposes. Our primary goal is to improve patient care. We hope to accomplish this in the short term by helping clinicians know and better understand the evidence (or lack of evidence) that determines current practice. By making this guideline broadly applicable, our purpose is to also encourage and enable the establishment and development of transplant programs worldwide. Finally, by providing comprehensive evidence-based recommendations, this guideline will also help define areas where evidence is lacking and research is needed. Helping to define a research agenda is an often neglected, but very important function of clinical practice guideline development.We used the GRADE system to rate the strength of evidence and the strength of recommendations. In all, there were only 4 (2%) recommendations in this guideline for which the overall quality of evidence was graded 'A,' whereas 27 (13.6%) were graded 'B,' 77 (38.9%) were graded 'C,' and 90 (45.5%) ' and 148 (74.7%) graded '2.' There were 3 (1.5%) recommendations graded '1A,' 16 (8.1%) were '1B,' 18 (9.1%) were '1C, ' and 13 (6.6%) were '1D.' There was 1 (0.5%) graded '2A,' 11 (5.6%) were '2B,' 59 (29.8%) were '2C, ' and 77 (38.9%) BackgroundExcept perhaps for transplantation between identical twins, all kidney transplant recipients (KTRs) need immunosuppressive medications to prevent rejection. Induction therapy is treatment with a biologic agent, either a lymphocyte-depleting agent or an interleukin 2 receptor antagonist (IL2-RA), begun before, at the time of, or immediately after transplantation. The purpose of induction therapy is to deplete or modulate T-cell responses at the time of antigen presentation. Induction therapy is intended to improve the efficacy of immunosuppression by reducing acute rejection, or by allowing a reduction of other components of the regimen, such as calcineurin inhibitors (CNIs) or corticosteroids. Available lymphocytedepleting agents include antithymocyte globulin (ATG), antilymphocyte globulin (ALG) and monomurab-CD3. Basiliximab and daclizumab, the two IL2-RAs that are currently available in many parts of the world, bind the CD25 antigen (interleukin-2 [IL2] receptor a-chain) at the surface of activated T-lymphocytes and thereby competitively inhibit IL2-mediated lymphocyte activation, a crucial phase in cellular immune response of allograft rejection. Rationale• There is high-quality evidence that the benefits of IL2-RA vs. no IL2-RA (or placebo) outweigh harm in a broad range of KTRs with variable immunological risk and concomitant immunosuppressive medication regimens.• There is moderate-quality evidence that a lymphocytedepleting agent vs. no lymphocyte-depleting a...

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Section: Rationalementioning

confidence: 99%

Special Issue: KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients

Eckardt¹,

Kasiske²,

Zeier³

2009

American Journal of Transplantation

1,205

294

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“…Reports of immunofluorescence have been in patients with gout and co-existent kidney disease, including cellular rejection and transplant glomerulopathy following renal transplantation [114], or drug-induced glomerulonephritis [115]. In patients with membranous nephropathy and gout, granular deposits of IgG, C3 and renal tubular epithelium antigen were observed in the glomerular capillary wall [108].…”

Section: Resultsmentioning

confidence: 99%

The anatomical pathology of gout: a systematic literature review

Towiwat

Chhana

Dalbeth

2019

BMC Musculoskelet Disord

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Background The aim of this systematic literature review was to comprehensively describe the anatomical pathology of tissues affected by gout. Methods We searched PubMed, The Cochrane Library, Excerpta Medica Database (EMBASE), and Web of Science Core Collection for all English language articles published before March 2018. Articles were included if they described the microscopic or macroscopic appearances of gout in human tissue. Results Four hundred and seventeen articles met inclusion criteria and were included in the review. Articles describing the anatomical pathology of gout in musculoskeletal structures, including bone, tendon and ligaments, synovium and cartilage, were most common. Articles describing skin and kidney pathology in gout were also common, with pathology in other sites such as visceral organs less common. At all sites, monosodium urate crystal deposition was reported, and the tophus was also described within many different tissues. During a gout flare, diffuse acute neutrophilic synovial inflammation was evident. The tophus was described as an organised chronic giant cell granulomatous structure consisting of monosodium urate crystals, innate and adaptive immune cells, and fibrovascular tissue. Conclusions Consistent with the clinical presentation of gout, most studies describing the anatomical pathology of gout report involvement of musculoskeletal structures, with monosodium urate crystal deposition and tophus the most common lesions described. This review details the anatomical pathology features of gout at affected sites. Electronic supplementary material The online version of this article (10.1186/s12891-019-2519-y) contains supplementary material, which is available to authorized users.

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“…In most cases hy peruricemia was asymptomatic; however, in some reports 7-11% of cases had clinical symptoms of gout [14,15]. Venkataseshan et al [16] described a case of kidney trans plant failure with graft loss, due to acute hyperuricemic nephropathy while on CyA therapy. Hyperuricemia in patients on CyA is caused by a tubular urate transport defect.…”

Section: Discussionmentioning

confidence: 99%

Effect of Nifedipine on Tubular Handling of Uric Acid in Transplanted Kidney on Cyclosporine A Treatment

Zawadzki¹,

Grenda²,

Januszewicz³

1995

Nephron

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Hyperuricemia resulting from tubular urate transport defects is a well-known nephrotoxic effect of cyclosporine A (CyA) on renal blood perfusion in organ recipients. The aim of this study was to define the mechanism of the tubular urate transport defect in hyperuricemic renal graft recipients on CyA and to evaluate the effect of nifedipine retard administration on this tubular dysfunction. Tubular uric acid transport was evaluated by the probenecid test in 17 hyperuricemic (group 1) and 6 normouricemic (group 2) renal graft recipients treated with CyA. Maximal urate excretion after probenecid administration was 25.5 ± 4.6 versus 42.5 ± 7.7% (p < 0.001) and postsecretory urate reabsorption was 79.2 ± 8.3 versus 78.5 ± 9.7% (NS), respectively. The effects of nifedipine retard on renal urate transport were evaluated in 6 hyperuricemic patients. Seven days of nifedipine therapy did not significantly decrease mean serum uric acid levels (7.7 ± 1.6 to 7.1 ± 1.1 mg/dl) nor increase urate clearance (3.8 ± 1.3 to 4.7 ± 1.6 ml/min/1.73 m²). The uricosuric effect of probenecid was manifested by an increase in tubular urate transport from 25.5 ± 4.6 to 37.3 ± 7.2%, p < 0.01, paralleled by an increase in postsecretory urate reabsorption from 20.5 ± 3.7 to 31.4 ± 5.7% (p < 0.003). Postsecretory reabsorption expressed as a percentage of secreted urate in both evaluations did not differ significantly (80.3 ± 6.2 vs. 84.4 ± 3.1%). These results suggest that hyperuricemia in kidney recipients on CyA is a consequence of decreased tubular urate secretion, and administration of nifedipine retard in these patients equally increased both tubular secretion and back-reabsorption of secreted uric acid.

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Acute Hyperuricemic Nephropathy and Renal Failure after Transplantation

Cited by 11 publications

References 8 publications

Special Issue: KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients

Special Issue: KDIGO Clinical Practice Guideline for the Care of Kidney Transplant Recipients

The anatomical pathology of gout: a systematic literature review

Effect of Nifedipine on Tubular Handling of Uric Acid in Transplanted Kidney on Cyclosporine A Treatment

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