Publications by authors named "Nnonyelum Onuigbo"

Background: Cardiac disease remains the major cause of death among ESRD patients. Indeed, the risk of cardiovascular events in ESRD is reported to be at least 3.4 fold higher than that of the general population.

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Hemodialysis (HD) exposes end-stage renal disease patients to significantly higher risks for Hepatitis B Virus (HBV) infection, a major public health scourge. Therefore, current US CDC guidelines, last revised in 2001, call for monthly HbsAg tests. The charge to Medicare per HbsAg test is $100.

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The syndrome of non-dilated obstructive uropathy (NDOU) and acute renal failure (ARF) is well reported. However, the literature suggests that this syndrome is rare, accounting for less than 5% of cases of urinary obstruction. Our recent experience with three cases of NDOU seen within a space of months implies otherwise.

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Concerns have been raised regarding a possible link between the increasing utilization of RAAS blocking strategies in the United States and the increasing ESRD epidemic. Most reports of accelerated renal failure in CKD patients with renal artery stenosis on RAAS blockade are retrospective. We hypothesized that this syndrome is therefore poorly understood, may be under-recognized, and demanded prospective analysis.

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Despite proven renoprotection from RAAS blockade and its increased application since the early 1990s, we have experienced an increasing CKD/ESRD epidemic, especially among U.S. diabetics.

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Contrast induced nephropathy, a leading cause of new-onset renal failure in U.S. hospitals, may be accelerated by concurrent RAAS blockade in CKD patients.

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Introduction: Notwithstanding proven renoprotection from RAAS blockade (AB) with ACE inhibitors and ARBs, and despite increasing utilization of AB in the US, we have continued to experience a CKD/ESRD epidemic. Given concerns for iatrogenic CKD/ESRD, we designed a prospective study to analyze the course of eGFR following withdrawal of AB in such patients.

Patients: Between September 2002 and February 2005, all consecutive CKD patients on AB presenting with >25% increase in baseline serum creatinine were enrolled.

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Background: Worsening azotemia following initiation of angiotensin blockade (AB), in patients with CKD, RAS with/without precipitating factors is recognized. Small increases in serum creatinine following initiation of AB occur and must not warrant drug discontinuation. We anecdotally had observed improvement in CKD in patients with normal renal arteries and no precipitating factors, following termination of AB.

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