Robert C. Albright

BACKGROUND: Survival is poor in patients with acute myocardial infarction (MI) who also have severe renal disease. Less is known about the outcome of acute MI in patients with mild to moderate renal insufficiency. OBJECTIVE: To compare outcomes after acute MI in patients with varying levels of renal disease and in patients without renal failure. DESIGN: Retrospective cohort study. SETTING: Academic medical center. PATIENTS: 3106 total patients admitted with acute MI and end-stage renal disease (n = 44), severe renal insufficiency (creatinine clearance < 0.59 mL/s [<35 mL/min]) (n = 391), moderate renal dysfunction (creatinine clearance > or = 0.59 mL/s [<35 mL/min] but < or =0.84 mL/s [< or =50 mL/min]) (n = 491), mild chronic renal insufficiency (creatinine clearance > 0.84 mL/s [>50 mL/min] but < or =1.25 mL/s [< or =75 mL/min]) (n = 860), or no renal disease (n = 1320). MEASUREMENTS: Clinical characteristics, treatment strategies, and short- and long-term survival were compared after patients were stratified by creatinine clearance. RESULTS: In-hospital mortality rates were 2% in patients with normal renal function, 6% in those with mild renal failure, 14% in those with moderate renal failure, 21% in those with severe renal failure, and 30% in those with end-stage renal disease (P < 0.001). Compared with patients without renal disease, similar adjusted trends were present for postdischarge death in patients with end-stage renal disease (hazard ratio, 5.4 [95% CI, 3.0 to 9.7]; P < 0.001), severe renal insufficiency (hazard ratio, 1.9 [CI, 1.2 to 3.0]; P = 0.006), moderate renal dysfunction (hazard ratio, 2.2 [CI, 1.5 to 3.3]; P < 0.001), and mild chronic renal insufficiency (hazard ratio, 2.4 [CI, 1.7 to 3.3]; P < 0.001). Patients with renal failure received adjunctive and reperfusion therapies less frequently than those with normal renal function (P < 0.001). Postdischarge death was less likely in patients who received acute reperfusion therapy (odds ratio, 0.7 [CI, 0.6 to 0.9]), aspirin (odds ratio, 0.7 [CI, 0.5 to 0.8]), and beta-blocker therapy (odds ratio, 0.7 [CI, 0.6 to 0.9]). CONCLUSION: Patients with renal failure are at increased risk for death after acute MI and receive less aggressive treatment than patients with normal renal function.

BACKGROUND AND OBJECTIVES: The arteriovenous fistula (AVF) is the preferred hemodialysis access, but AVF-failure rate is high, and complications from AVF placement are rarely reported. There is no clear consensus on predictors of AVF patency. This study determined AVF outcomes and patency predictors at Mayo Clinic Rochester following the Fistula First Initiative. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: A retrospective cohort study of AVFs placed at Mayo Clinic from January 2006 through December 2008 was performed. The AVF placement-associated primary and secondary failure rates, complications, interventions, and hospitalizations were examined. Kaplan-Meier survival curves and Cox proportional hazard models were used to determine primary and secondary patency and associated predictors. RESULTS: During this time frame, 317 AVFs were placed in 293 individual patients. The primary failure rate was 37.1% after excluding patients not initiated on hemodialysis during follow-up (n = 38) or those with indeterminate outcome (37 lost to follow-up; six died; two transplanted). Of usable AVFs, 11.4% later failed. AVF creation incurred complications and hospitalization in 21.2% and 12.3% of patients, respectively. The risk for reduced primary patency was increased by diabetes (HR, 1.54; 95% CI, 1.14 to 2.07); the risk for reduced primary and secondary patency was decreased with larger arteries (HR, 0.83; 95% CI, 0.73 to 0.94; and HR, 0.69; 95% CI, 0.56 to 0.84, respectively). CONCLUSIONS: Primary failure remains a major issue in the post-Fistula First era. Complications from AVF placement must be considered when planning AVF placement. Our data demonstrate that artery size is the main predictor of AVF patency.

Letters1 August 2006Nephrogenic Fibrosing Dermopathy and High-Dose Erythropoietin TherapySundararaman Swaminathan, MBBS, Iftikhar Ahmed, MD, James T. McCarthy, MD, Robert C. Albright, DO, Mark R. Pittelkow, MD, Noel M. Caplice, MD, PhD, Matthew D. Griffin, MB BCh, and Nelson Leung, MDSundararaman Swaminathan, MBBSFrom Mayo Clinic College of Medicine, Rochester, MN 55905., Iftikhar Ahmed, MDFrom Mayo Clinic College of Medicine, Rochester, MN 55905., James T. McCarthy, MDFrom Mayo Clinic College of Medicine, Rochester, MN 55905., Robert C. Albright, DOFrom Mayo Clinic College of Medicine, Rochester, MN 55905., Mark R. Pittelkow, MDFrom Mayo Clinic College of Medicine, Rochester, MN 55905., Noel M. Caplice, MD, PhDFrom Mayo Clinic College of Medicine, Rochester, MN 55905., Matthew D. Griffin, MB BChFrom Mayo Clinic College of Medicine, Rochester, MN 55905., and Nelson Leung, MDFrom Mayo Clinic College of Medicine, Rochester, MN 55905.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-145-3-200608010-00021 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Background: Nephrogenic fibrosing dermopathy is a newly described cutaneous disorder characterized by mucin deposition and dermal infiltration of CD34+ spindle cells in patients with renal insufficiency (1). No etiologic factor besides kidney disease has been linked to this disorder, although CD34 is a marker of hematopoietic progenitor cells. Erythropoietin is the principal therapy for anemia in both dialysis and predialysis patients. Its use dramatically increased after the publication of the Dialysis Outcomes Quality Initiative guidelines for anemia management in 1997 (2). Of interest, this is the same year that the first case of nephrogenic fibrosing dermopathy was reported (3).Objective: ...References1. Cowper SE. Nephrogenic fibrosing dermopathy: the first 6 years. Curr Opin Rheumatol. 2003;15:785-90. [PMID: 14569211] CrossrefMedlineGoogle Scholar2. NKF-DOQI clinical practice guidelines for the treatment of anemia of chronic renal failure. National Kidney Foundation-Dialysis Outcomes Quality Initiative. Am J Kidney Dis. 1997;30:S192-240. [PMID: 9339151] MedlineGoogle Scholar3. Cowper SE, Robin HS, Steinberg SM, Su LD, Gupta S, LeBoit PE. Scleromyxoedema-like cutaneous diseases in renal-dialysis patients [Letter]. Lancet. 2000;356:1000-1. [PMID: 11041404] CrossrefMedlineGoogle Scholar4. LeBoit PE. What nephrogenic fibrosing dermopathy might be [Editorial]. Arch Dermatol. 2003;139:928-30. [PMID: 12873893] CrossrefMedlineGoogle Scholar5. Macdougall IC. Antibody-mediated pure red cell aplasia (PRCA): epidemiology, immunogenicity and risks. Nephrol Dial Transplant. 2005; 20 Suppl 4 iv9-15. [PMID: 15827058] CrossrefMedlineGoogle Scholar6. Drueke T. Hyporesponsiveness to recombinant human erythropoietin. Nephrol Dial Transplant. 2001; 16 Suppl 7 25-8. [PMID: 11590253] CrossrefMedlineGoogle Scholar7. Haroon ZA, Amin K, Jiang X, Arcasoy MO. A novel role for erythropoietin during fibrin-induced wound-healing response. Am J Pathol. 2003;163:993-1000. [PMID: 12937140] CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From Mayo Clinic College of Medicine, Rochester, MN 55905.Disclosures: None disclosed. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoErythropoietin, Gadolinium, and Nephrogenic Fibrosing Dermopathy Richard N. Hellman Erythropoietin, Gadolinium, and Nephrogenic Fibrosing Dermopathy Nelson Leung , Sundararaman Swaminathan , Iftikhar Ahmed , James T. McCarthy , Robert C. Albright , Mark R. Pittelkow , Noel M. Caplice , and Matthew D. Griffin Metrics Cited byNephrogenic Systemic Fibrosis as a Complication after Gadolinium-Containing Contrast Agents: A Rapid ReviewFibrotic Signaling Pathways of Skin Fibroblasts in Nephrogenic Systemic FibrosisToxicité rénale des produits de contraste non iodésNephrogenic Systemic FibrosisMagnetic Resonance Imaging for Interventions and SurgeryThe role of gadolinium chelates in the mechanism of nephrogenic systemic fibrosis: A critical updateMRI for Interventions and SurgeryGadolinium Contrast Agent-Induced CD163+ Ferroportin+ Osteogenic Cells in Nephrogenic Systemic FibrosisEvaluation of imatinib mesylate as a possible treatment for nephrogenic systemic fibrosis in a rat modelSafety of Older Generations of Gadolinium in Mild-to-Moderate Renal FailureCutaneous Manifestations of Renal DiseaseInsuffisance rénale chronique et dialyseToxic MetalsUnderstanding Nephrogenic Systemic FibrosisNephrogenic systemic fibrosis is found only among gadolinium‐exposed patients with renal insufficiency: a case–control study from DenmarkFibrose systémique néphrogéniqueNephrogenic Systemic Fibrosis and Gadolinium-Based Contrast AgentsQuantification of gadolinium in fresh skin and serum samples from patients with nephrogenic systemic fibrosisRevisiting nephrogenic systemic fibrosis in 6 kidney transplant recipients: A single-center experienceTransmetallation and gadolinium: Do low iron stores prevent the development of nephrogenic systemic fibrosis in high-risk end-stage renal disease patients?Disorders of Connective TissueThe Outcome of Patients with Nephrogenic Systemic Fibrosis after Successful Kidney TransplantationRapid improvement of nephrogenic systemic fibrosis with rapamycin therapy: Possible role of phospho-70-ribosomal-S6 kinaseNephrogenic systemic fibrosis with a spectrum of clinical and histopathological presentation: a disorder of aberrant dermal remodelingA Difficult Airway in a Patient with Nephrogenic Sclerosing FibrosisNephrogenic systemic fibrosis: What 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Recognition and TreatmentNSF: WHAT WE KNOW AND WHAT WE NEED TO KNOW: Patient Characteristics and Risk Factors for Nephrogenic Systemic Fibrosis Following Gadolinium ExposureNephrogenic Systemic FibrosisLocalized nephrogenic fibrosing dermopathy: Aberrant dermal repairing?Scleroderma-like Fibrosing DisordersExtracorporeal photopheresis improves nephrogenic fibrosing dermopathy/nephrogenic systemic fibrosis: Three case reports and review of literatureImaging agentsNephrogenic systemic fibrosisThe Impact of NSF on the Care of Patients With Kidney DiseaseNephrogene systemische Fibrose (NSF) nach Applikation gadoliniumhaltiger Kontrastmittel bei ShuntpatientenNephrogenic systemic fibrosis: Center case reviewEvaluating the role of recombinant erythropoietin in nephrogenic systemic fibrosisNephrogenic systemic fibrosis: a case series suggesting gadolinium as a possible aetiological factorNephrogenic systemic fibrosis: A nephrologist's perspectiveGadolinium Is Not the Only Trigger for Nephrogenic Systemic Fibrosis: Insights From Two Cases and Review of the Recent LiteratureNephrogenic systemic fibrosis and gadolinium-based contrast agentsNew Insights into Nephrogenic Systemic FibrosisThe Role of the Hospital Dermatologist in the Diagnosis and Treatment of Calciphylaxis and Nephrogenic Systemic FibrosisRisk Factors for Developing Gadolinium-Induced Nephrogenic Systemic FibrosisNephrogenic systemic fibrosisNephrogenic Systemic Fibrosis, Gadolinium, and Iron MobilizationDermopathie néphrogénique fibrosante traitée par photochimiothérapie extracorporelle : rôle du gadolinium ?Gadolinium and nephrogenic systemic fibrosisNephrogenic systemic fibrosis: A clinicopathologic study of six casesFibrose systémique néphrogénique et produits de contraste IRM à base de sels de gadolinium: quelle imagerie pour l'insuffisant rénal chronique?Nephrogenic systemic fibrosis: is any contrast safe in renal failure?Conventional or Gadolinium containing contrast media: the choice between acute renal failure or Nephrogenic Systemic Fibrosis?Safety update on the possible causal relationship between gadolinium-containing MRI agents and nephrogenic systemic fibrosisNephrogenic Systemic Fibrosis: A Mysterious Disease in Patients with Renal Failure—Role of Gadolinium-Based Contrast Media in Causation and the Beneficial Effect of Intravenous Sodium ThiosulfateErythropoietin, Gadolinium, and Nephrogenic Fibrosing DermopathyRichard N. Hellman, MDCurrent awareness: Pharmacoepidemiology and drug safetyGadolinium is detectable within the tissue of patients with nephrogenic systemic fibrosis 1 August 2006Volume 145, Issue 3Page: 234-235KeywordsAttentionBody weightCellsErythropoietinHematopoietic stem cellsHemoglobinMedical dialysisParathyroid hormoneResearch laboratoriesSerum ferritin levels ePublished: 1 August 2006 Issue Published: 1 August 2006 Copyright & PermissionsCopyright © 2006 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...

Despite being an anabolic hormone in skeletal muscle, insulin's anticatabolic mechanism in humans remains controversial, with contradictory reports showing either stimulation of protein synthesis (PS) or inhibition of protein breakdown (PB) by insulin. Earlier measurements of muscle PS and PB in humans have relied on different surrogate measures of aminoacyl-tRNA and intracellular pools. We report that insulin's effect on muscle protein turnover using aminoacyl-tRNA as the precursor of PS and PB is calculated by mass balance of tracee amino acid (AA). We compared the results calculated from various surrogate measures. To determine the physiological role of insulin on muscle protein metabolism, we infused tracers of leucine and phenylalanine into 18 healthy subjects, and after 3 h, 10 subjects received a 4-h femoral arterial infusion of insulin (0.125 mUxkg(-1)xmin(-1)), while eight subjects continued with saline. Tracer-to-tracee ratios of leucine, phenylalanine, and ketoisocaproate were measured in the arterial and venous plasma, muscle tissue fluid, and AA-tRNA to calculate muscle PB and PS. Insulin infusion, unlike saline, significantly reduced the efflux of leucine and phenylalanine from muscle bed, based on various surrogate measures which agreed with those based on leucyl-tRNA (-28%), indicating a reduction in muscle PB (P < 0.02) without any significant effect on muscle PS. In conclusion, using AA-tRNA as the precursor pool, it is demonstrated that, in healthy humans in the postabsorptive state, insulin does not stimulate muscle protein synthesis and confirmed that insulin achieves muscle protein anabolism by inhibition of muscle protein breakdown.