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Progression of non-diabetic chronic renal failure
Başlık:
Progression of non-diabetic chronic renal failure
Yazar:
Mackinnon, Bruce, author.
ISBN:
9780438058996
Yazar Ek Girişi:
Fiziksel Tanımlama:
1 electronic resource (240 pages)
Genel Not:
Source: Dissertation Abstracts International, Volume: 76-08C.
Advisors: Jonathan Fox.
Özet:
There is an alarming growth in the prevalence of chronic renal failure (CRF) and end stage renal disease (ESRD) worldwide which shows no sign of abating. The global population of dialysis patients in 2001 was estimated to be 1.5 million. With a projected increase of at least 7% per year, this will have reached 2 million in 2005 and 2.5 million in 2010.1 This is an important issue, not only for those afflicted by renal disease, but also for society at large, as this patient group consumes a disproportionate fraction of the total healthcare budget. One way of attempting to reverse this trend is to reduce the incidence of common causes of ESRD such as diabetes, another is to study individuals who have already developed CRF in the hope that new insights into the way their disease progresses will leads us to new therapeutic targets to slow, halt, or even reverse the progression of CRF. There is a widely held belief among nephrologists, that the progression of renal impairment occurs in a linear fashion. However, this would not be in keeping with Brenner's 'hyperfiltration theory' which would suggest that an accelerating decline in GFR should follow initial renal injury. Using a large database of patients with biopsy- proven IgA nephropathy we have shown, not only that a single model cannot be applied to progression in all individuals, but also that progression appears to occur more often in a linear than in a non-linear manner. When it was first recognised 30 years ago that proteinuria often heralded a future decline in GFR, this was attributed to its association with more severe glomerular injury. More recently, evidence has emerged which suggests that, in fact, proteinuria may directly lead to renal injury and a decline in GFR. The nature of this relationship remains unclear. In an effort to address this question, a cohort of individuals with proteinuric renal impairment secondary to a variety of glomerular and interstitial nephropathies was recruited. After collecting spot urine samples from each, urinary transferrin was measured. Urine proteins were also separated by SDS gel electrophoresis into low, medium and high molecular weight bands. On following this group over a mean period of 20 months, it was found that quantity of urinary protein in the high molecular weight bands (> 100 kDa) was independently correlated with rate of change in estimated creatinine clearance, whereas urinary transferrin (mol wt. 69 kDa) was not. The diagnosis of analgesic associated nephropathy (AAN) remains controversial and not all nephrologists accept its existence as a separate entity. There are no universally accepted criteria for diagnosis, nor any unifying theory to explain its pathogenesis. It has been shown here that patients identified as suffering from AAN, due to a prolonged history of ingestion of multiple analgesics, and after exclusion of other causes for their renal impairment, are more likely to die or progress to ESRD if they continue taking analgesics. In addition to ongoing use of analgesics, male gender and baseline proteinuria were identified as independent correlates of the rate of change in estimated creatinine clearance.
Notlar:
School code: 0547
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Yer Numarası | Demirbaş Numarası | Shelf Location | Lokasyon / Statüsü / İade Tarihi |
---|---|---|---|
XX(684676.1) | 684676-1001 | Proquest E-Tez Koleksiyonu | Arıyor... |
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