About Me

Until I moved to Arizona in 2002, I had lived on islands all my life. There was Manhattan (yes, that’s an island), Long Island, and Staten Island.  I miss the water, but not enough to move back to the cold.

As a New York native, I earned my B.A. (‘69) in English and M.A. (‘72) in Communications from Hunter College of CUNY. I minored in Secondary Education.

I’m not a doctor.  I wasn’t even interested in medical issues until I was diagnosed with Chronic Kidney Disease in 2008. Before then, I took advanced courses in writing and computers.

Until I retired from teaching for the fourth and final time in 2013, I taught fairly steadily. NYC high schools and colleges were my original stomping grounds, but when I relocated to the Southwest, I taught only college. There were various literature, writing, grammar, and literary history courses.  Research writing was one of my favorites.

I retired from acting that year, too.  I had a wonderful time with this for over forty years, but finally had to admit to myself that I no longer could keep an entire script in my memory for stage nor did I have the stamina for early calls and long days of shooting for film. I don’t know if it was CKD or age, but something was in the way and it simply wasn’t fun anymore.

One thing I haven’t given up is writing.  I’ve been a non-fiction writer for over thirty years (maybe that’s why I so enjoyed teaching research writing) for venues as diverse as The New York City Board of Education and The National Kidney Foundation. I earned an Academic Certificate in Creative Writing from Rio Salado College in 2011 and have started adding fiction to my writing resume. Take a look at Portal in Time on Amazon.com and B&N.com. Don’t let anyone fool you: fiction is harder to write than fact.

My other passion is advocacy for Chronic Kidney Disease Awareness. Since I was diagnosed (stage 3 and holding), I’ve written  What Is It and How Did I Get It? Early Stage Chronic Kidney Disease; The Book of Blogs: Moderate Stage Chronic Kidney Disease, Part 1; The Book of Blogs: Moderate Stage Chronic Kidney Disease, Part 2; SlowItDownCKD – 2015 and SlowItDownCKD – 2016. (All available on Amazon.com and B&N.com.)I’ve been hosted for book signings in all sorts of places, and monitored kidney talks (once even in a TwitterChat). I’ve been interviewed on Renal Diet Headquarters, Online with Andrea, Working with Chronic Disease, Improving Your Health, the Author Show and by Tufts School of Medicine.

I’ve been honored to write for The National Kidney Foundation, Kidney Steps, Is What It Is, Kevin MD, and Kidney Times. The Wall Street Journal, Glendale Community College’s ‘Gaucho Gazette,’ and The NephCure Foundation have all featured articles on both my books and advocacy. I post a daily CKD tidbit on SlowItDownCKD‘s Facebook page, too.

And the blog, we mustn’t forget the blog. This venture began after a doctor from India, whose name I’ve long forgotten, contacted me to tell me he wanted the book for his patients, but they couldn’t even afford the bus fare to the clinic. That’s when I got the bright idea to print each chapter as a weekly blog.  He would then translate and print it to give to the patients who were able to make it to the office.  It was free and he felt they would share it with the other CKD patients they knew. And then I just kept blogging.

My wonderfully supportive husband and I have separate offices, a must to keep our love alive.  In our combined family, we have two adult daughters who live nearby, another in New York (who occasionally guest blogs here), and a fourth currently living in California.  The finishing touch to our family is Shiloh, a rescue dog who has become Bear’s constant companion.

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Published on March 8, 2014 at 9:59 pm  Comments (6)  

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6 CommentsLeave a comment

  1. This is great! Nice to read the backstory. And you have an impressive one!

  2. Thank you, Vanessa. As I wrote it, I realized all over again how much I love my life.

    Let’s see what we can do about getting SlowItDown working in California!

  3. I was just diagnosed, after being misdiagnosed for over 6 years! Terrified, I still have 3 teens in the home.

    • I recognize your feelings, having felt them myself when I was diagnosed, but CKD is not a death sentence. What stage are you? I would suggest reading my book (big surprise here) and any others like it you can find so you can write a list of questions for your nephrologist. I’ve been at stage 3A for six years and have no intention of letting this go farther. Are you aware of the CKD support groups on Facebook? Rest, follow the renal diet, exercise at least half an hour a day, and (gulp!) relax. Remember I’m not a doctor, but I am a CKD patient.

      Relax just enough to catch your breath. Then start researching.

  4. Gail: You may not have seen this in the New England Journal of Medicine so I forward it FYI; keep up your good work!

    Dr. Nick

    Teaching Topics | July 3, 2014
    Acute Kidney Injury and Chronic Kidney Disease: What is considered to be the most important risk factor for acute kidney injury?

    JOURNAL EDITORIAL FELLOW
    The Journal invites applications from medical professionals at any career stage for a one-year, full-time, paid editorial fellowship beginning in July 2015. The editorial fellow will work on Images in Clinical Medicine and other Journal features and will participate in the day-to-day editorial activities of the Journal. In addition, the fellow will undertake an independent project of his or her choosing. Deadline for applications is September 1, 2014. Please see the Now@NEJM blog for more information.

    Teaching Topic
    Acute Kidney Injury and Chronic Kidney Disease
    REVIEW ARTICLE
    Acute Kidney Injury and Chronic Kidney Disease as Interconnected Syndromes
    L.S. Chawla and Others
    CME Exam
    During the past decade, separate conceptual models for chronic kidney disease and acute kidney injury were developed to facilitate organized approaches to clinical research and trials. Recent epidemiologic and mechanistic studies suggest that the two syndromes are not distinct entities but rather are closely interconnected — chronic kidney disease is a risk factor for acute kidney injury, acute kidney injury is a risk factor for the development of chronic kidney disease, and both acute kidney injury and chronic kidney disease are risk factors for cardiovascular disease.

    Clinical Pearls
    Clinical Pearl What is considered to be the most important risk factor for acute kidney injury?
    Multiple risk factors for acute kidney injury are now known to include advanced age, diabetes mellitus, and black race. Similar risk factors have been identified for chronic kidney disease. However, the most important risk factor for acute kidney injury is preexisting chronic kidney disease, which increases risk by as much as 10 times, as compared with the absence of chronic kidney disease.

    Figure 1. Acute Kidney Injury and Chronic Kidney Disease as an Interconnected Syndrome.

    Clinical Pearl How does acute kidney injury impact the risk of developing chronic kidney disease?
    Several findings suggest that acute kidney injury not only is directly linked to the progression of chronic kidney disease but causes chronic kidney disease as well. First, the increased severity of acute kidney injury is associated with the development of chronic kidney disease. Second, multiple episodes of acute kidney injury predict the development of chronic kidney disease.

    Morning Report Questions
    Q. What is the association between acute kidney injury or chronic kidney disease and cardiovascular disease?
    A. In addition to being associated with chronic kidney disease, acute kidney injury is linked to the development and treatment of cardiovascular disease. A strong association between chronic kidney disease and an increased risk of cardiovascular events is well documented. Patients who survive an episode of acute kidney injury are also at risk for major adverse cardiovascular events, as well as for progression to chronic kidney disease, regardless of whether there is underlying cardiovascular disease. Patients with acute kidney injury after coronary angiography are at risk for hospitalization for cardiovascular causes, myocardial infarction, and vessel reocclusion; the severity of acute kidney injury has been associated with hospitalization for heart failure. Acute kidney injury is associated with higher rates of death or subsequent hospitalization for stroke, heart failure, or myocardial infarction than the rates associated with previous myocardial infarction.

    Figure 1. Acute Kidney Injury and Chronic Kidney Disease as an Interconnected Syndrome.

    Q. What are strategies for management after an episode of acute kidney injury?
    A. Patients with acute kidney injury should have periodic assessment of renal function and the urinary albumin-to-creatinine ratio to assess prognosis and outcome after discharge. The appropriate treatment for patients who survive an episode of acute kidney injury, regardless of whether they have chronic kidney disease, is unclear. Reasonable therapeutic approaches to patients who do not have preexisting kidney disease but do have evidence of renal injury include, first, “do no harm,” by avoiding nephrotoxic medications, including nonsteroidal antiinflammatory drugs and radiocontrast agents. In addition, one needs to determine the appropriate treatment for important risk factors for chronic kidney disease such as diabetes and hypertension. The preventive use of inhibitors of the renin–angiotensin–aldosterone system, low-sodium diets, or both should be evaluated in such patients. The authors note that it is not known whether these therapeutic approaches ameliorate or worsen outcomes in patients with acute kidney injury or in those with combinations of acute kidney injury and chronic kidney disease. Patients who have had acute-on-chronic episodes of acute kidney injury and chronic kidney disease should be followed by primary care physicians as well as nephrologists to ensure the highest standards of care.

    Teaching Topic
    Giant-Cell Arteritis and Polymyalgia Rheumatica
    CLINICAL PRACTICE
    Giant-Cell Arteritis and Polymyalgia Rheumatica
    C.M. Weyand and J.J. Goronzy
    CME Exam Full Text Audio Comments
    Giant-cell arteritis is an inflammatory vasculopathy that typically occurs in medium and large arteries with well-developed wall layers and adventitial vasa vasorum. The vascular beds that are usually affected include the external carotid branches (e.g., temporal and occipital arteries), the ophthalmic, vertebral, distal subclavian, and axillary arteries, and the thoracic aorta. Polymyalgia rheumatica causes aching and stiffness in selected muscle groups, predominantly in the neck, shoulders, upper arms, and pelvic girdle. Symptoms are most pronounced in the morning.

    Clinical Pearls
    Clinical Pearl What is the epidemiology of giant-cell arteritis and polymyalgia rheumatica, and how often do the diagnoses overlap?
    Giant-cell arteritis and polymyalgia rheumatica have multiple risk factors and pathogenic abnormalities in common. Approximately 50% of patients with giant-cell arteritis present with polymyalgia rheumatica before, at the time of, or after the diagnosis of vasculitis. Symptoms of polymyalgia rheumatica often appear when the therapy for giant-cell arteritis is being tapered. Both giant-cell arteritis and polymyalgia rheumatica are diseases that affect the elderly, with a peak incidence at the age of 70 to 80 years; age (50 years or older) is considered a criterion for the diagnosis. Women account for 65 to 75% of patients. Polymyalgia rheumatica occurs at a frequency that is 3 to 10 times that of giant-cell arteritis.

    Clinical Pearl What are laboratory results in patients with giant-cell arteritis and polymyalgia rheumatica?
    Marked elevations in the erythrocyte sedimentation rate (ESR) and the level of C-reactive protein (CRP) are common in giant-cell arteritis and polymyalgia rheumatica, as are the presence of thrombocytosis and anemia. In a cohort of 764 patients with suspected giant-cell arteritis who underwent biopsy, with the diagnosis confirmed in 177 patients, the sensitivity of an elevated ESR was 84% and that of an elevated CRP level was 86%; the specificity of these markers was low, however, at 30%. Only 4% of patients with confirmed giant-cell arteritis had both a normal ESR and a normal CRP level at the time of diagnosis. Assessment of inflammatory markers is helpful during diagnostic evaluation and long-term monitoring, but elevated levels of these markers should not be the only indication for immunosuppressive therapy. No highly specific biomarkers for giant-cell arteritis and polymyalgia rheumatica have been validated.

    Morning Report Questions
    Q. What is the standard for diagnosis of suspected giant-cell arteritis?
    A. In cases of suspected giant-cell arteritis, histologic verification of vasculitis should be sought by means of a temporal-artery biopsy with assessment of a vascular segment that is 1.5 to 2.0 cm in length. Histologic analysis is the standard for diagnosis; it can detect small inflammatory infiltrates and can also distinguish giant-cell arteritis from non–giant-cell arteritis arteritides (e.g., ANCA-associated vasculitis). High-field-strength MRI may emerge as a method that is sensitive to the detection of temporal-artery inflammation, but neither ultrasonography nor MRI has yet replaced temporal-artery biopsy, which is highly sensitive for even minor inflammatory changes.

    Q. What is the optimal treatment for giant-cell arteritis and polymyalgia rheumatica?
    A. Giant-cell arteritis and polymyalgia rheumatica are responsive to glucocorticoids. Most treatment recommendations are based on clinical experience rather than the results of randomized, controlled trials. Therapy for giant-cell arteritis is initiated with prednisone at a dose of 1 mg per kilogram of body weight per day. Given the risk of irreversible ischemic complications, new-onset clinical manifestations of disease indicating an unstable supply of blood to the eyes or the central nervous system (e.g., arteritic optic neuropathy) are typically managed with intravenous pulse therapy (e.g., 1000 mg of methylprednisolone per day for 3 consecutive days) to optimize immunosuppression and suppress tissue edema. The doses of glucocorticoids used to treat polymyalgia rheumatica are much lower than those used for the treatment of giant-cell arteritis. In the majority of patients, a dose of 15 to 20 mg of prednisone per day is sufficient to control myalgia. No glucocorticoid-sparing agents have been approved for the treatment of giant-cell arteritis or polymyalgia rheumatica.

    Archive of Teaching Topics »

    • Thanks for thinking of me, Nick. I made sure to include the journal’s website and a direct link to this particular article in last week’s blog.


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