Diff'rent Looks

May 15 2012 Published by under Kidney Function

The first time I thought about pediatric kidney disease occurred my senior year of high school. That fall Diff'rent Strokes debuted, introducing Gary Coleman as Arnold Jackson, a precocious, wise-cracking 7-year-old from Harlem.

Pediatric kidney disease, 1978

Arnold sometimes seemed wise beyond his years. Of course, he was being played by 10-year-old Gary Coleman who looked far younger than his chronological age. Thanks to focal segmental glomerulosclerosis (FSGS), a particularly nasty form of childhood nephrotic syndrome, and attempts to treat it, Gary's growth was stunted. His adult height measured 4 feet 7 inches, so he could play much younger characters...up to a point. He received two kidney transplants, both of which failed due to recurrent kidney disease.

The entire child cast of the show subsequently led troubled lives. Gary Coleman died in 2010 of a brain hemorrhage.

This week the face of pediatric kidney failure changed when Sarah Hyland, the older sister on Modern Family, revealed that she has lived with chronic kidney disease her entire 20 years of life. She recently received a kidney transplant from her father during the show's summer filming hiatus. 

Pediatric kidney disease, 2012

Lucky for Sarah, she had a much different condition called dysplasia. During development, her kidneys failed to form enough normal tissue to support her throughout her life. Doctors diagnosed her slowly-progressive condition at 9 years of age. She never received the high-dose steroids that gave Gary Coleman his round face. She benefited from decades of research that dramatically improved the ways we manage the growth failure and bone disorders that can accompany all kidney diseases. She will likely have excellent function from her father's kidney for many years without the appearance-altering side effects of earlier anti-rejection drugs.

We have made a lot of progress, but we need to make more. FSGS has some new treatments, but many patients still fail to respond and develop permanent kidney failure. FSGS still recurs in the transplant, killing the new kidney as it did the native ones. Dysplasia does not develop in the transplant, but other conditions may shorten the life of the replacement kidney. The side effects of anti-rejection drugs may be less visible, but their risks of infection, diabetes, and cancer still raise problems. We still have a lot of research to do.

But in my lifetime, look at the progress we have made!

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Poison by Any Other Name

Apr 05 2012 Published by under [Medicine&Pharma]

Evil chemicals! Click for source

What image springs to mind when you see the word...

nicotine?

If you smoke, you may have a warm, fuzzy feeling, but for a lot of us, poison comes to mind. Nicotine makes tobacco products addictive, so it cannot be good. See the diagram at right; it's used as an insecticide! It kills bugs! It must be bad!

Of course, nicotine is merely a chemical. But chemicals are bad, right? Even a natural one that comes from a plant (like tobacco)? Even one with a short, pronounceable name?

So nicotine is bad...except when it isn't.

Renoprotective effects of long-term oral nicotine in a rat model of spontaneous proteinuria.
Agarwal et al. Am J Physiol Renal Physiol 302:F895, 2012
DOI:  10.1152/ajprenal.00507.2011

Nicotine has demonstrated beneficial effects in a number of inflammatory disorders, including inflammatory bowel disease, sepsis, and hypersensitivity pneumonitis. In animal models of ischemia-reperfusion kidney injury results are more variable, depending on the model and route of nicotine administration. It seems that macrophages (immune white blood cells) and capillaries in the kidney have alpha-7 nicotinic acetylcholine receptors which modulate these anti-inflammatory effects.

This study used a rat model of spontaneous proteinuria, Munich-Wistar-Fromter rats. As these rats age, they develop proteinuria. As protein is reabsorbed by the peritubular capillaries in the kidney, filtered agents such as cytokines and growth factors can promote inflammation and further kidney damage. At the time proteinuria begins in this model (24 weeks, a middle-aged rat), animals were begun on one of three doses of nicotine in drinking water along with an untreated control group. Saccharine in the water in all groups masked the taste of nicotine (yes, the control rats were drinking diet soda, circa 1970). Every 4 weeks they measured blood pressure, glomerular filtration rate, and proteinuria. They examined kidney structure in a number of ways after 28 weeks of study, when the rats reached one year of age.

Kidney function (upper panel) & proteinuria (lower panel)

The control rats showed the typical course for the MWF model, with glomerular filtration rates less than half of baseline after 28 weeks of study (see figure at left). This effect on clearance of waste products was blunted by nicotine ingestion. Protein excretion increased in all groups of rats, but, once again, nicotine treatment reduced the level of protein spill.

Nicotine treatment also reduced scarring in the glomeruli, the filtering units of the kidneys. Macrophages, those pesky blood cells that promote inflammation and scarring, were also reduced by nicotine treatment. Production of scar materials by the kidney was also reduced with the nicotine treatment.

So proteinuric patients should smoke? Or at least wear those patches?

Not exactly.

Smoking is a major risk factor for the development and progression of all sorts of kidney diseases. We ABSOLUTELY DO NOT WANT ANYONE SMOKING EVER FOR ANY REASON!

Like most molecules, nicotine has many faces. In this case, we examined its perky, anti-inflammatory side. Nicotine also has other effects that may not be desirable. Short-term ingestion raises blood pressure and heart rate via stimulation of the adrenergic system; these effects were not detected with long-term ingestion in this rat model. Nicotine also affects a number of systems that modulate blood flow (and can therefore affect function) of the kidney. Changes in these systems were not assessed in the present study.

Also, prior studies show that what happens in rats does not necessarily happen in mice when it comes to nicotine. Why? We really do not know. Do these species metabolize nicotine differently? Or is there some other reason for these differences? When it comes to nicotine, are people more like rats or mice or neither?

Nicotine has another danger: addiction. Can we come up with a modified nicotine (with a longer, scarier, more chemically name) that would provide anti-inflammatory effects without producing undesirable vascular or behavioral effects? Anything is possible, but this molecule is still in the future.

The bottom line: nicotine from a natural, plant-based source like tobacco can be a killer. Pure nicotine from the lab may be a healer. Only time and more experiments will tell.

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I Beg to Differ: Diabetes in the US

Mar 20 2012 Published by under [Medicine&Pharma]

Ronald Ricker posted today about upcoming physician shortages and our failure to deal with them. In his writing he considers a number of improvements in health that have increased our lifespans substantially over the past 150 years. His key message, that we are not training enough physicians, is good. I disagree strongly with one of his assertions:

The discovery of insulin by Banting, Best, et. al. largely wiped out the scourge of diabetes.

Before Banting's work, what we now call type 1 diabetes mellitus produced a rapid death by starvation. Some patients could hang on for months on a diet of fat and protein, but without insulin replacement the Reaper came knocking before too long. Insulin allowed these patients to metabolize carbohydrates and survive. In 1921, it seemed the scourge of type 1 diabetes had been wiped out.

Of course, most patients with diabetes mellitus have always had the less dramatic, insidious type 2. This form usually occurs in older individuals, often in association with obesity and insulin resistance. Kimmelstiel and Wilson published the first description of the pathology of diabetic kidney disease in 1936 (PDF here). The discovery of insulin allowed those with type 1 diabetes to live long enough to develop this condition, as well as other complications of the hyperglycemic state. Today, despite improvements in glycemic control, approximately 40% of patients with diabetes of any type will develop kidney complications. Diabetes has become the leading cause of permanent kidney failure in the US, producing 154 new cases per million population per year. Nearly 1,800 people out of every million in the US have permanent kidney failure; of these, over 1/3 suffered this fate from diabetes (see figure from US Renal Data Service).

From USRDS

Insulin seemed miraculous to the children and young adults who developed type 1 disease; however, its discovery did not cure this condition, nor did it "wipe out the scourge." Instead an acute fatal illness became a chronic disease, much like the type 2 form. We ended up with more people living with diabetes.

We still need more research on diabetes and its complications. Better metabolic control, via an artificial pancreas or islet transplants, could potentially cure type 1 diabetes. Type 2 disease, where the initial issue is usually insulin resistance, will not be cured through these endeavors. We need to understand more about how the complications of diabetes, including kidney failure, blindness, nerve damage, gastrointestinal dysfunction, and cardiovascular disease, develop and progress. Why do only 40% of patients get kidney damage from diabetes? What makes one person vulnerable while another patient remains protected?

It has been more than 3 decades since microalbuminuria, the first clinical marker of diabetic kidney disease was reported. Over that time, we have discovered important flaws in its specificity and sensitivity - so we really don't have a marker of early kidney disease! We have not developed an effective new treatment in more than 20 years. I would say we are overdue.

Recent reports in the Journal of the American Society of Nephrology suggest that circulating receptors for TNF alpha may provide a more useful biomarker of risk. It would be a big step forward for research (and patient care in the future), but it is not enough. Unfortunately, recent hits to the NIH budget mean fewer physicians and scientists will be studying these diseases (and a multitude of others).

In short, insulin saved lives, but the scourge of diabetes is still going strong.

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Am I Science? Yes, #IamScience

Jan 30 2012 Published by under Women in Medicine, Women in Science, [LifeTrajectories]

Compared to the other stories posting via this meme, I feel almost traditional.

I do not remember a time when science was not part of my life. I recall fondly reading and re-reading All About Dinosaurs. I had a tiny kit containing most of the minerals in Moh's scale. Mom refused to complete my set with her jewelry, so I had to imagine the upper levels of hardness. Biology clearly won my heart, though. How things could be alive fascinated me to no end.

Unlike many scientists, I was not the outdoorsy type. I read fashion magazines, did a bit of modeling, and entered some teen-queen pageants. I often joke that a hotel without 24-hour room service is my idea of camping. I love air conditioning and indoor plumbing; I fail to see how doing without these conveniences constitutes "fun." This quirk effectively ruled-out a career in paleontology or biological field work. I do love people. Having a father in academia, and coming of age during the 1970's PhD glut, teachers suggested aiming for an MD which guaranteed employment.

Click for source

Admission to medical school was fiercely competitive in that era, and I aimed my sights on a relatively new program at the University of Missouri - Kansas City. The medical curriculum began on day 1 out of high school and went 11 months each year for 6 years. Getting in meant avoiding the cut-throat competition among pre-med students on many campus. Its goal when pitched to the legislature was producing primary care physicians for under-served areas of Missouri, not academic physician-scientists. My second year there, I got a work-study job as a lab assistant for a fresh-out-of-post-doc carcinogenesis researcher needing cheap labor. This year provided my first experience with real science as I worked with the doctoral student and another lab to set up our efforts. Everyone, including this 19-year-old part-timer, needed to generate data. I learned to do short-term lymphocyte cultures, murine surgery, and a number of assays. The principal investigators of these labs strongly suggested that I figure out a way to pick up a PhD to go with my MD, since I loved the science so much.

The next few years brought more intensive courses and clinical work with overnight call, making meaningful lab time improbable if not impossible. I love science, but another kind of love intervened, along with a big princess wedding. By the time I graduated with my BA and MD, the idea of getting another advanced degree sounded exhausting and unnecessary. I headed off to pediatric residency with the intention of becoming a hematologist-oncologist, building on my background in carcinogenesis. Of course, I met a whole bunch of nephrologists and their patients who convinced me to take my talents elsewhere. After all, urine is golden!

My first 6 months of fellowship were a gray blur. Post-partum depression plus a prolonged period of call without a break left me feeling bleak. January in Minnesota is not exactly rosy, but I entered a lab and felt alive again. More than 100 patients with diabetes of various stages had kidney biopsy material stored for study. I began to ask questions about diabetic kidney disease, learning to do electron microscopy along the way. I published papers, completed my training, and landed a faculty position. National funding followed, along with a better position in Omaha, a great place to live and raise our offspring.

Eventually, my science hit the wall. One project just would not work, no matter what we tried. Another project got shot down by reviewer 3 at the same time the NIH budget tanked. I realized that I could not write a better grant than what I had submitted. The probability of getting the funding expected at my professional level was incredibly close to zero. Even efforts with smaller agencies to get funding for pilot data failed, as these foundations cut back support to established investigators during the recession.

The kids left the nest, and my hubby had an amazing job offer in a warmer town. We moved on last year, and I am turning my problem solving skills back to the clinic and to research in faculty development. I still have a grad student back in Nebraska (who is proving reviewer 3 wrong; take that!), and I love the chance to talk science on a regular basis. I do not miss the grant pressure or knowing that several other people will be out of a job if I fail.

Am I still science? When I see a patient, I gather data through a history and physical exam. I create a hypothesis as to what I believe is wrong, and I test that diagnosis through laboratory studies or treatment. If I am wrong, I go back, readjust my hypothetical diagnosis, and test again. Sounds like the scientific method to me.

I may not have a full-time lab. I may not be a funded PI. I still believe that I am science - with incredible fashion sense, of course.

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Back Again?

Dec 30 2011 Published by under [Medicine&Pharma]

One bad form of kidney disease, membranoproliferative glomerulonephritis (we docs call it MPGN), may be "enjoying" a resurgence. Since I have not seen a case for a few years, an update seems in order. I pulled a 2011 review by Howard Trachtman, a pediatric nephrologist at the Albert Einstein College of Medicine.

Click for original source with more information

MPGN is inflammation of the filtering units of the kidney (glomerulonephritis or GN) that occurs with activation of the complement system of immunity. Other forms of GN that do this  include post-streptococcal GN and systemic lupus erythematosus. A number of secondary causes of complement activation and MPGN include chronic liver disease, cryoglobulinemia, and subacute bacterial endocarditis. These disorders may result in circulating immune complexes that lead to complement activation.

Kidney biopsy is the only way to make the diagnosis. (For a 9-minute review of normal kidney structure, click here.) The "membrano" part of the name refers to characteristic changes in the glomerular basement membrane (GBM) of the filtering capillaries (see arrow in micrograph). Abnormal material "splits" the GBM and fills this space, giving a duplicated or tram-track appearance on light microscopy. Mesangial cells multiply (or "proliferate"), completing the name. Other studies demonstrate components of the complement system depositing within the glomeruli.

Click for source and as much as you ever want to know about complement

What is the complement system? Glad you asked!  Complements form a protein-based immune response (see figure above). In the classical pathway, an antigen-antibody complex activated C1 which activates C4, and so on, ultimately consuming C3 and/or C5, resulting in a membrane attack complex (MAC) that can, well, attack the membrane of the foreign invader. The alternate pathway activates C3 directly with the same end result, often via contact with a surface that can adsorb the complement component. Clinical laboratories usually measure C3, C4, and a measure of total complement consumption. If C4 is low, then the classical pathway has been stimulated; C3 may be suppressed as well. If C4 remains normal with a low C3, the alternative pathway is the culprit.

The primary form of MPGN is a rare disease, affecting 1 to 2 per million population per year. Unlike many kidney diseases, MPGN is "equal-opportunity" and does not disproportionately affect any ethnicity or gender. The disorder tends to be slowly progressive, with approximately half of affected patients requiring replacement of kidney function within 5-10 years. The prognosis and course does not differ for children and adults with MPGN. Less than 5% of patients with permanent kidney failure have this as the cause. Three forms have been described:

  • Type 1: Subendothelial deposits (between the cells lining the capillaries and the GBM)
  • Type 2: Large, ribbon-like intramembranous deposits (dense deposit disease); this form has a somewhat worse prognosis and is associated with partial lipodystrophy in ~25% of cases
  • Type 3: Subendothelial (like type 1) and subepithelial deposits (between the foot processes and the GBM)

In addition to the kidney biopsy, patients need lab studies for hepatitis, cryoglobulinemia, and complements: C3, C4, and C3 nephritic factor. The latter, an autoantibody to C3bBb, is positive in 60-70% of patients with type 2 disease, but only 20% of other types.

At this time, treatment for MPGN includes normalizing blood pressure and reducing proteinuria as with all chronic kidney disorders. In children, immunosuppression with oral steroid every other day for several years may retard progression of disease; in adults, steroids are not recommended. If a secondary cause of MPGN is demonstrated, treatment of that disorder may also benefit the kidney involvement. The development of drugs that specifically target complement activation (eculizumab) offer novel options to explore in these rare forms of GN.

Kidney tranplant can be performed in these patients, but the disease may recur in the graft. Once again, type 2 disease fares worse with 80-90% risk of recurrence, compared to ~30% in those with the other forms. MPGN can be a persistent pest.

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Rhythm of Life

Dec 02 2011 Published by under [Medicine&Pharma]

Check out my Guest Post over at Scientific American today: Dipping with the Stars.

If the video player doesn't show above, click here for a real visual treat.
Sadly, I'm not talking about that sort of dipping or those sorts of stars. No, this post discusses what your blood pressure does when you sleep at night while the stars shine in the sky.

Enjoy your weekend!

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Taking Slow, Deliberate Baby Steps

Nov 03 2011 Published by under [Information&Communication], [Medicine&Pharma]

I cannot understand why biomedical jounals (with rare exceptions) do not have places online for discussion of articles. How many people actually get their act together to write a formal letter to the editor, especially when that sort of publication counts for next to nothing on your CV?

In contrast, a lively discussion can occur in the blogosphere if you do not place too many barriers to participation.

I think the American Society of Nephrology finally gets it!

In the last couple of weeks they quietly rolled out an interactive blog with Disqus sign-in for comments. Yesterday the ASN overlords tweeted about the site, so it's now fair game for me to blog. Yes, the ASN tweets; over the past year they have established an active social media presence in a number of venues.

Normotensive Dipper (Click to Enlarge)

Hypertensive NonDipper (Click to Enlarge)

Now they've built it, and we should click! The latest post regards a study showing that bedtime administration of blood pressure medications in chronic kidney disease patients significantly reduces the risk of stroke and cardiovascular events. Why should that be? Well, normal people have an overnight "dip" in blood pressure while they sleep (upper image at left). Even patients with hypertension may retain a "dip" and have a better prognosis than patients who lose the dip. Many hypertensive patients lose their "dip" (lower image), sometimes even before their daytime blood pressures become elevated!

Overnight level of hypertension and lack of "dip" indicates greater cardiovascular risk than daytime blood pressure levels. Giving at least one dose of antihypertensive therapy at bedtime can lower overnight blood pressure and restore a more normal physiological (dare I say circadian?) pattern.

So click over and help get some chat going on the site if you care about kidneys and related science and policy. It's also an example of how mainstream journals can open up for discussion without the risk that their official site will get cluttered with spam and trolls.

Keep this effort in mind for ScienceOnline2012. On Saturday at noon I will facilitate (at an un-conference do I un-facilitate or obstruct?) the discussion on the resistance of journals and media to blogging and online post-publication review of the scientific record. See you in North Carolina!

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New Data; Now What?

Sep 12 2011 Published by under Journal Club

One of the most common reasons children get sent to see me is persistent microscopic hematuria. In non-doctor-talk, they have red blood cells in their urine that can only be detected by dipstick or microscope. The prevalence of children affected is not clear, but less than 1% in most studies where at least 3 urine specimens are checked.

My approach has been fairly laid-back. Most children with significant kidney disease warranting intervention have some other indicator, such as gross hematuria (visible with the naked eye), protein in the urine, high blood pressure, and/or an abnormal glomerular filtration rate (GFR, the measurement of how the kidneys clear waste products). In the absence of these findings, or other abnormalities on blood tests, the probability of finding a treatable, progressive disorder on biopsy remains very low. These children warrant follow-up every year or two so that biopsy and treatment can be reconsidered if other signs or symptoms develop.

When the following article hit the news, I knew it would impact my life:

Persistent Asymptomatic Isolated Microscopic Hematuria in Israeli Adolescents and Young Adults and Risk for End-Stage Renal Disease.

Click to embiggen

Vivante A, et al. JAMA 2011; 306:729-36

All Jewish Israeli adolescents and young adults must undergo medical board examination 1 year before conscription into military service. All screened participants from 1975 - 1997 were included in the study. The recruitment schema is shown at left. The investigators then linked these records to the Israeli end-stage renal disease registry to look at outcomes in these subjects.

One of the powers of this study is its numbers. Well over one million individuals underwent initial screening, and 1,199,936 ultimately did not have persistent microscopic hematuria or other risk factors for kidney disease (Control Group). Some screened individuals had diabetes or other conditions putting them at risk of kidney failure (34,243), while 3,690 (0.3%) met the criteria for isolated microscopic hematuria after multiple urinalyses with microscopic examination, kidney and bladder imaging studies, and measurement of serum creatinine level. All of these subjects visited a nephrologist who confirmed the diagnosis.

People with hematuria were twice as likely to be male as female. No differences in country of origin, blood pressure, or body size were identified at military screening.

Click to embiggen

After a median follow-up of 20 years, end-stage kidney failure developed in 539 people without hematuria (0.045%) and in 26 patients with hematuria (0.7%), an approximately 20-fold elevation in risk.  The cause of kidney failure in hematuria patients was mostly glomerular disorders including IgA nephropathy (see table at right). Hematuria patients had lower body mass index, younger age at start of kidney failure therapy, and shorter time to kidney failure than those who developed kidney failure without preceding hematuria. Multivariate analysis revealed no mediating factors that changed these relationships.

The risk of end-stage kidney failure was 2.05 per 100,000 person-years in the Control Group and 34.0 in the hematuria group. While this represents a substantial increase in relative risk, the absolute risk remains low when compared with other chronic diseases. These hematuria patients produced 4.3% of treated end-stage kidney failure during the study period.

There are some problems with this study. First, the study population is limited, and results may not generalize to other patient groups. Second, historical evaluation techniques may not produce the same diagnoses as those of today. Intravenous pyelography was the standard for imaging in the first part of the study; ultrasound replaced it over time. Proteinuria screening has also changed; today, the more sensitive measurement of microalbuminuria might skew some patients out of the isolated hematuria group. Also, the only assessment of kidney function available was a nephrologist's statement that the serum creatinine was "normal." Calculated GFR might also have altered some of these results.

The real question is how should these data alter current medical practice? For now, I do not believe they should. The patients I see have documented persistent microscopic hematuria. We screen for a variety of systemic and glomerular disorders up front. We use state-of-the-art imaging for anatomic abnormalities, and we measure microalbuminuria to look for very low levels of proteinuria. These children then get followed-up annually, either with a primary care physician or in our office. If any other signs or symptoms of kidney disease develop, we perform a biopsy. Still, we fail to make a diagnosis or find a treatable illness in many cases.

The other question raised is the use of screening urinalysis. Data from Japan's childhood screening program suggest that an aggressive approach may reduce the risk of kidney failure due to glomerular diseases in that country. At this point, it remains unclear if more screening or biopsies would prevent enough end-stage kidney failure to justify the expense and risk of  the procedure, especially when the risk is low (even though the relative risk is high).

 

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Foolish Choices Cost Lives and Money

Jun 09 2011 Published by under MedicoLegal Concerns

Click for source

The June 9 issue of New England Journal of Medicine includes a Perspective piece from a nephrologist and hospitalist at the county hospital in Houston, TX. They discuss an issue well-known to those of us in the nephrology community, the care of illegal immigrants with kidney failure. Kidney disease strikes a disproportionate number of ethnic minorities, including those of African, Hispanic, and Native American Ancestry.

US citizens qualify for public funding for their dialysis and transplants, either through the Medicare or Medicaid programs. Federal law prohibits the use of federal funds for non-emergency services for undocumented residents. Raghavan and Nuila describe the plight of these people:

Santiago is in the ER again. He sits in a special row of 20 patients, all of whom are waiting for one result: the potassium. Is it high enough today? Two days ago he was here, and it was only 6 meq per liter. We discharged him. Right now his chest hurts, and he is short of breath. Nothing new, and Santiago knows that if he's to be dialyzed today, these symptoms don't matter. Only the potassium matters.

Thrice weekly hemodialysis, the current standard-of-care for citizens, costs $72,000 per patient per year. Some would argue that this regimen is inadequate, that we should be providing more dialysis to improve patient outcomes, but many of these patients can work and live reasonable lives. Emergency dialysis for undocumented residents places the lives of these people at risk, as well as resulting in ER visits and hospitalizations for emergencies that must be paid for by our public hospitals (using local and state tax dollars and subsidized by increasing charges to other patients). Total costs average $200,000 annually for each of these emergency-dialysis patients.

My direct experience deals with the children without papers, who came to this country with their parents. Sometimes the families can save and fund-raise and get their children transplanted, although then they must bear the burden of the costs of immunosuppression for the rest of their lives. Sometimes good parents allow their children to become wards of the state so they can get the medical care that will give them better lives.

The examples that Raghavan and Nuila provide illustrate the problems of current policy. People who came to this country illegally, but to work hard to support families, can no longer work because of the inadequate care they receive for their conditions. This inadequate care not only prevents them from contributing to the economy via their work, purchases, and sales taxes, but ends up costing the public more than if we provided standard in-center dialysis. The authors admit that this issue "lies at the intersection of debates over the soaring cost of health care and the need for immigration reform."

Do we have an ethical duty to provide the same standard of care for all sick patients within our borders? Or would mandating the providion of health care (and of maintenance-dialysis treatments) create an incentive for illegal immigration and worsen the current situation?

There is no easy solution. But with this particular disease, there are cheaper, more compassionate alternatives...

They make an excellent case for the foolishness of our current choices. Should we let these people die of their disease? Should we continue to provide our current torture care at almost 3 times the cost of standard care? Or can we come up with a more effective and cost-effective scheme for dealing with this problem?

Note: This article is not live on the NEJM site as I schedule this post; I will add a direct link to the text later on June 9. And that link is now live.

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What I Am Reading: Kidney Edition

Jun 01 2011 Published by under Uncategorized, What I'm Reading

Click to buy

Walter A. Hunt's new book fills a niche in the kidney disease market: a book by a patient about living with the knowledge that your kidneys will fail, living with failed kidneys, and surviving it all to get transplanted. The subtitle, A Guide for Living, sums it up nicely; you can survive and thrive with kidney disease. In this age of self-help and patients empowerment, it seems impossible that no one has written this book before now. Unfortunately, Walter A. Hunt is not a typical kidney disease patient (more on that later), so the book may not have as broad an audience as possible.

The book flows in the predicted fashion, from what kidneys do and why they fail, though the diagnostic tests and treatment options available at each step of the way. Throughout the book, the author remembers that each patient's disease will be different, and that no single prescription can fit everyone, especially before the onset of end-stage kidney failure. Personal insights on adapting and dealing with issues may be of benefit to many patients, especially if they lack an understanding support system.

My major criticism of the book stems from the author's background. Dr. Hunt holds a doctorate in neuropharmacology and performed biomedical research for 30 years before his diagnosis with polycystic kidney disease. While this background certainly helped him understand his condition, the writing in the book likely exceeds the health literacy of much of the population. Terms like "diffuse" may not be familiar to the average kidney patient (even though I am certain most heard it in a science class somewhere along the way), but clearly he assumes that word will be understood:

Dialysis involves filtration. Start with a basic concept: imagine a tank of water into which you carefully place a drop of ink in one corner of the tank. The concentrated ink tends to diffuse over time throughout the entire container of water until it reaches the same concentration in all parts of the tank.

Starting with a definition of diffusion might have been useful for the average adult in the US.

Kidney Disease: A Guide for Living may not be a perfect guide for patients, but it fills an empty slot on the patient's bookshelf. Motivated patients may find it a valuable addition to their kidney disease management tools.

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