Uric Acid Lowering to Prevent Kidney Function Loss in Diabetes: PERL Allopurinoal Study

Author(s)

Dr Mujtaba Ali Hasnain , Dr Zubair Anwar , Dr Abdul Rehman ,

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Volume 9 - October 2020 (10)

Abstract

Significant morbidity and mortality is caused by diabetic kidney disease in people around the globe with type 1 diabetes. Previously, intensive focus was on blood pressure and glucose control which proved to be less effective and as a failure in preventing the progression of the disease and curbing it. Multiple studies have shown the significance of lowering uric acid levels in treating diabetic kidney disease and preventing its progression. This review paper includes a trial conducted by the Preventing Early Renal Function Loss (PERL0 Consortium using allopurinol, in lowering the uric acid level and stating that such novel interventions much be tested for positive outcomes. Although the trial targeted diabetes type 1 patients, but the use or allopurinol as a renoprotective agent was found effective in a large number of population. It is inexpensive, safe to use and is cost effective for patients who are at lower risk and going through initial disease stages

Keywords

Uric Acid, Kidney Function loss

References

                 i.            Marshall SM. Diabetic nephropathy in type 1 diabetes: has the outlook improved since the 1980s? Diabetologia. 2012;55(9):2301–6. [PubMed] [Google Scholar]

      ii.            Nathan DM, Zinman B, Cleary PA, et al. Modern-day clinical course of type 1 diabetes mellitus after 30 years’ duration: the diabetes control and complications trial/epidemiology of diabetes interventions and complications and Pittsburgh epidemiology of diabetes complications experience (1983–2005) Arch Intern Med. 2009;169(14):1307–1316. [PMC free article] [PubMed] [Google Scholar]

    iii.            Krolewski AS, Bonventre JV. High risk of ESRD in type 1 diabetes: new strategies are needed to retard progressive renal function decline. Semin Nephrol. 2012;32(5):407–414. Review highlighting the need for new strategies and novel therapeutics to prevent renal function decline. [PMC free article] [PubMed] [Google Scholar]

     iv.            Maahs DM, Rewers M. Editorial: Mortality and renal disease in type 1 diabetes mellitus--progress made, more to be done. J Clin Endocrinol Metab. 2006;91(10):3757–3759. [PubMed] [Google Scholar]

       v.            de Boer I, Rue TC, Hall YN, Heagerty PJ, Weiss NS, Himmelfarb J. Temporal trends in the prevalence of diabetic kidney disease in the United States. JAMA. 2011;305(24):2532–2539. Overview of prevalence of DKD in the US and demonstrates continued burden of diabetic kidney disease on individuals and its public health importance.

     vi.             Bilous R, Chaturvedi N, Sjolie AK, et al. Effect of candesartan on microalbuminuria and albumin excretion rate in diabetes: three randomized trials. Ann Intern Med. 2009;151(1):11–14. [PubMed] [Google Scholar]

   vii.             Mathiesen ER, Hommel E, Giese J, Parving HH. Efficacy of captopril in postponing nephropathy in normotensive insulin dependent diabetic patients with microalbuminuria. BMJ. 1991;303(6794):81–87. [PMC free article] [PubMed] [Google Scholar]

 viii.             Parving HH, Brenner BM, McMurray JJ, et al. Cardiorenal End Points in a Trial of Aliskiren for Type 2 Diabetes. N Engl J Med. 2012 In Press Recent clinical trial highlighting the need for novel therapeutics to improve cardiorenal health in people with diabetes.

     ix.             Jalal DI, Maahs DM, Hovind P, Nakagawa T. Uric acid as a mediator of diabetic nephropathy. Semin Nephrol. 2011;31(5):459–465. [PMC free article] [PubMed] [Google Scholar]

       x.             Edwards NL. The role of hyperuricemia and gout in kidney and cardiovascular disease. Cleve Clin J Med. 2008;75 (Suppl 5):S13–S16.

     xi.             Becker MA, Schumacher HR, Jr, Wortmann RL, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. 2005;353(23):2450–2461. [PubMed] [Google Scholar]

   xii.             Schumacher HR, Jr, Becker MA, Wortmann RL, et al. Effects of febuxostat versus allopurinol and placebo in reducing serum urate in subjects with hyperuricemia and gout: a 28-week, phase III, randomized, double-blind, parallel-group trial. Arthritis Rheum. 2008;59(11):1540–1548. 

 xiii.             Jung JW, Song WJ, Kim YS, et al. HLA-B58 can help the clinical decision on starting allopurinol in patients with chronic renal insufficiency. Nephrol Dial Transplant. 2011;26(11):3567–3572. [PubMed] [Google Scholar]

 xiv.             Lonjou C, Borot N, Sekula P, et al. A European study of HLA-B in Stevens-Johnson syndrome and toxic epidermal necrolysis related to five high-risk drugs. Pharmacogenet Genomics. 2008;18(2):99–107. [PubMed] [Google Scholar]

   xv.             Tassaneeyakul W, Jantararoungtong T, Chen P, et al. Strong association between HLA-B*5801 and allopurinol-induced Stevens-Johnson syndrome and toxic epidermal necrolysis in a Thai population. Pharmacogenet Genomics. 2009;19(9):704–709. Pharmacogenetic data in which the association of HLA-B*5801 is identified as an important risk factor for SJS . 

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