User blog: Meguid El Nahas
Urinary Sodium and Potassium Excretion and CKD Progression.
CKD is a major risk factor for ESRD, cardiovascular disease, and premature death. Whether dietary sodium and potassium intake affect CKD progression remains unclear. We prospectively studied the association of urinary sodium and potassium excretion with CKD progression and all-cause mortality among 3939 patients with CKD in the Chronic Renal Insufficiency Cohort Study. Urinary sodium and potassium excretion were measured using three 24-hour urine specimens, and CKD progression was defined as incident ESRD or halving of eGFR. During follow-up, 939 CKD progression events and 540 deaths occurred. Compared with the lowest quartile of urinary sodium excretion (<116.8 mmol/24 h), hazard ratios (95% confidence intervals) for the highest quartile of urinary sodium excretion (≥194.6 mmol/24 h) were 1.54 (1.23 to 1.92) for CKD progression, 1.45 (1.08 to 1.95) for all-cause mortality, and 1.43 (1.18 to 1.73) for the composite outcome of CKD progression and all-cause mortality after adjusting for multiple covariates, including baseline eGFR. Additionally, compared with the lowest quartile of urinary potassium excretion (<39.4 mmol/24 h), hazard ratios for the highest quartile of urinary potassium excretion (≥67.1 mmol/24 h) were 1.59 (1.25 to 2.03) for CKD progression, 0.98 (0.71 to 1.35) for all-cause mortality, and 1.42 (1.15 to 1.74) for the composite outcome. These data indicate that high urinary sodium and potassium excretion are associated with increased risk of CKD progression. Clinical trials are warranted to test the effect of sodium and potassium reduction on CKD progression.
Interesting and not surprising observation linking a high urinary sodium excretion with CKD progression. The association seemd to be affected by the level of albuminuria that also correlated with the rate of CKD progression.
The authors showed the association to be independent of presence or absence of hypertension, type of anti-hypertensive agent or systolic blood pressure...
the association between high urinary sodium excretion, most likely the reflection of high dietary sodium intake, is most liley the refelction of poorly controlled hypertension...
the authors overlook the fact that a casual, occasional, single blood poressure recording is meaningless and doesnt ascertian whether individuals are hypertensive or not and/or controlled or not...
WHEN WILL NEPHROLOGISTS LEARN THAT CASUAL, SINGLE, BP READING DOESNT INFORM ON HYPERTENSION, ITS PRESENCE OR THE QUALITY OF ITS CONTROL...
This whole paper is likely to tell us that a high sodium diet, associated with a high urinary sodium excretion, increases BP, that in turn affects both albuminuria and the rate of CKD progression...no more or less!
On the 17th of September the New York Times published a well balanced account of the issue of kidney dysfunction in the growing elderly population, it was entitled:
Chronic Kidney Disease Can Be Dubious Diagnosis
and it highlighted the debate that rages amongst Nephrologists with on one hand those claiming an alarming rise in those affecetd by CKD; mostly the elderly population, and on the other hand those calling for moderation and consideration that such a high prevalence of "CKD" merely reflects the decline in kidney function with ageing and arguing against the medicalisation of old age...
The artilce received many congratulations and acclaims for its fair and balanced display of the two prevailing views.
The story doesnt stop here...with a fair and well reported medical item by a major newspaper of international repute and acclaim...
Pressure was brought to bear on the author of this excellent article by those who saw in the above title a bias...favoring those doubting the label of CKD in th eelderly population...leading her to change the title in subsequent editions to:
For Older Adults, Questioning a Diagnosis of Chronic Kidney Disease
whilst this is in itself surprising and disappointing, it highlights alarming facts:
1. The Press, even in the most advanced of democracies, gives in to lobbies and pressure...
2. The Press is not free to express its views and biases, unchecked by those who hold differing views...
3. The general and medical Press is hostage to pressure and lobbies that curtails its freedom of expression.
I though this was the domain of politics and political lobbies, this incident highlighted to me that medical reproting is equally hostage to pressure and gives in equally to lobbies and censure.
A VERY SAD DAY FOR MEDICAL REPORTING!
International guidelines adopted in 2012 make it seem that way. They define the disease in terms of how efficiently kidneys filter the waste from our blood, a measure called the glomerular filtration rate. Healthy young people commonly have G.F.R.s of about 120. A G.F.R. lower than 60 or another marker of kidney damage (such as protein in the urine) for more than three months means chronic kidney disease.
At which point, patients become scared. “When you’re told you have a disease, that’s a bad day,” said Dr. Ann O’Hare, a nephrologist at the University of Washington in Seattle who specializes in treating older adults. “Patients worry about dialysis, because that’s what they associate with kidney disease.”
Chronic kidney disease causes no symptoms until its later stages, and most seniors with the diagnosis are told they’re at Stage 3, of five — sudden, unwelcome news. Because Medicare uses these benchmarks for billing and reimbursement, they’ve become, in effect, the official definition of the disease for older Americans.
But wait a minute. Kidney function declines with age in almost everyone, and the proportion of older people with G.F.R. readings below 60 approaches 50 percent, studies have found. As the older adult population grows, the prevalence may rise even higher.
Yet the proportion of older people who will ever reach kidney failure, and thus need dialysis or a transplant, remains very low. People don’t turn to dialysis until their G.F.R. sinks much further, to about 10. In the great majority of older adults, that will never happen.
The lifetime risk of kidney failure in the United States is 3.6 percent for whites and 8 percent for African-Americans, one widely cited study found.
“Probably a majority of older patients we see have some degree of impaired renal function,” said Dr. Michael Steinman, a geriatrician at the University of California, San Francisco. “The chances are far and away that they’ll die of something else, and their kidneys will never be a problem.
“Why are we even thinking about this as a disease?”
Indeed, a small but spirited cadre of physicians and researchers are arguing — most recently in JAMA — that the guidelines should be recalibrated by age.
By using the same standards for everyone, ”We’re labeling and medicalizing and victimizing a substantial fraction of the elderly population,” said Dr. Richard Glassock, an author of the article and a nephrologist at the University of California, Los Angeles.
Instead, Dr. Glassock and others propose that in people older than 65, the diagnosis should require a G.F.R. reading less than 45. At that lower threshold, they estimate, a third to half of the chronic kidney disease diagnosed in older patients would suddenly disappear.
These patients should just be considered … old, the researchers say, with lower kidney function normal for their ages.
When it comes to kidney decline, Dr. O’Hare said, a G.F.R. below 60 would cause great concern in a 20-year-old. At older ages, “it’s a gray zone.”
Most G.F.R. readings that fall below 60 in older adults remain in the 45 to 59 range, considered a modest reduction in kidney function. Most of these seniors will not have protein in their urine or other evidence of kidney damage. “People are being told they have a condition and it doesn’t really mean anything,” Dr. O’Hare said.
In the same JAMA issue, though, another group of physician researcherswarned against changing the guidelines.
“Having chronic kidney disease increases the risk of death from any cause, but particularly cardiovascular disease,” a co-author, Dr. Andrew Levey, the chief of nephrology at Tufts Medical Center, said in an interview. “People with kidney disease shouldn’t be treated the same as people without it.”
Regarding kidney disease as part of normal aging offends researchers like Dr. Levey. They point out that although the relative risk of dying is actually higher in younger people with chronic kidney disease, the absolute risk — the numbers of people who die from it — is higher at older ages.
Moreover, they argue, an older person with low G.F.R. and protein in his urine (called proteinuria or albuminuria) can take some steps to reduce the risk of eventual kidney failure, even if that’s already extremely low. Certainblood pressure medications with tongue-tangling names may protect the kidneys, for instance, though their effect on older adults is also a matter of debate.
A diagnosis can also help patients avoid drugs that can harm kidneys, said Dr. Levey and the co-author Dr. Josef Coresh, an epidemiologist at Johns Hopkins Bloomberg School of Public Health. (Both were part of the working group that developed the guidelines.) Doctors can modify medication dosages and warn older patients away from drugs that can impair kidney function, like ibuprofen, certain injected antibiotics, and the contrast dyes used in CT scans.
Generally, though, what a doctor tells an older patient found to have chronic kidney disease is fairly standard counsel: Control your blood pressure, which exacerbates kidney disease and vice versa, and yourcholesterol. Manage your diabetes. Keep track of drugs.
“That’s just sensible, healthy living, whether you have kidney disease or not,” Dr. Glassock said. So he questions whether we should even call somewhat reduced kidney function at older ages a disease.
It may amount to more than semantics. Along with fears of sitting in a dialysis center three days a week for the rest of one’s life come the costs of additional tests, appointments and referrals to specialists. “It pulls people into further engagement with the health care system,” Dr. O’Hare said. Most older adults face plenty of that already.
Still, here’s the reality: Revising the international guidelines, a protracted and complicated undertaking, doesn’t appear to be in the cards. The definition we have is the one we’re going to have for years, maybe for good. Many older people are likely at some point to hear a physician say they have chronic kidney disease.
How should they respond?
No special screening is required to learn one’s glomerular filtration rate. It’s part of the common basic metabolic panel. Most of us have it in our records somewhere.
One thing the kidney disease combatants agree on is that a G.F.R. less than 60 should prompt a conversation, before any prescription or advice. Doctors need to put these numbers in perspective, to explain that kidneys age with the rest of us.
It makes sense to repeat the test to see if the G.F.R. remains stable or continues to fall; it also makes sense to test the urine for protein. Physicians can use risk predictors —some exist, more are coming — to help determine an individual’s odds of kidney failure.
That way, Dr. Levey said, “we’re identifying the patients at risk for the worst outcomes and reassuring the others.”
But reassurance should be by far the more common response, whether a physician uses the D-word or not.
“I don’t think this is something to lose sleep over,” Dr. O’Hare tells patients with modestly lower but stable G.F.R., and no other indications of kidney damage. “That’s often a huge relief.”
Those who argue that patients should be labelled as "DISEASED" to adjust medication dosage or to avoid another disease such as AKI...fly in the face of reality and commion sense.
Our job as doctors is to avoid and prevent diseases...NOT to mislabel people in the community as DISEASED...for the sake of PROTECTING THEM...
if this held true then, EVERYBODY OVER THE AGE OF 65 WOULD BE SOMEHOW "DISEASED"...weather it is lung "disease" due to reduced lung vital capacity..., heart "disease" due to reduced diastolic function.., Bone "disease" due to reduced bone mineral density, not to mention visual and hearing diseases...due to age-related reduced visual and hearing acuity...
IT IS HIGH TIME THE MEDICALISATION OF OLD AGE IS STOPPED NO MATTER HOW LUCRATIVE THIS MAY BE TO SOME...
CKD DEFINITION, CLASSIFICATION AND EPIDEMIOLOGY; IS IT ALL ABOUT MONEY...?!
In the US, labelling older people as suffering from CKD 3a (age related decline in kidney function) leads under the Medicare Advantage plans to enhanced reimbursements to large private medical groups; Defining and labelling older people as suffering from "CKD" leads under the HCC system to increased reimbursement.
All too often an older patient with years of stable eGFRs of let say 59ml/min gets suddenly labeled as “CKD stage 3a” to increase his healthcare provider's income...at the expense of burdening the patient with an unnecessary and unjustified diagnosis of "CKD".
THIS MUST STOP!
The CKD classification has to be revised to spare millions the mislabelling of "CKD" even if it costs millions to private healthcare providers in the US...
A new age-sensitive classification has to be adopted.
IT IS HIGH TIME WE STOP MIXING CKD AND BUSINESS...
5 year mortality predictors in 498 103 UK Biobank participants: a prospective population-based study.
To our knowledge, a systematic comparison of predictors of mortality in middle-aged to elderly individuals has not yet been done. We investigated predictors of mortality in UK Biobank participants during a 5 year period. We aimed to investigate the associations between most of the available measurements and 5 year all-cause and cause-specific mortality, and to develop and validate a prediction score for 5 year mortality using only self-reported information.
Participants were enrolled in the UK Biobank from April, 2007, to July, 2010, from 21 assessment centres across England, Wales, and Scotland with standardised procedures. In this prospective population-based study, we assessed sex-specific associations of 655 measurements of demographics, health, and lifestyle with all-cause mortality and six cause-specific mortality categories in UK Biobank participants using the Cox proportional hazard model. We excluded variables that were missing in more than 80% of the participants and all cardiorespiratory fitness test measurements because summary data were not available. Validation of the prediction score was done in participants enrolled at the Scottish centres. UK life tables and census information were used to calibrate the score to the overall UK population.
About 500 000 participants were included in the UK Biobank. We excluded participants with more than 80% variables missing (n=746). Of 498 103 UK Biobank participants included (54% of whom were women) aged 37-73 years, 8532 (39% of whom were women) died during a median follow-up of 4·9 years (IQR 4·33-5·22). Self-reported health (C-index including age 0·74 [95% CI 0·73-0·75]) was the strongest predictor of all-cause mortality in men and a previous cancer diagnosis (0·73 [0·72-0·74]) was the strongest predictor of all-cause mortality in women. When excluding individuals with major diseases or disorders (Charlson comorbidity index >0; n=355 043), measures of smoking habits were the strongest predictors of all-cause mortality. The prognostic score including 13 self-reported predictors for men and 11 for women achieved good discrimination (0·80 [0·77-0·83] for men and 0·79 [0·76-0·83] for women) and significantly outperformed the Charlson comorbidity index (p<0·0001 in men and p=0·0007 in women). A dedicated website allows the interactive exploration of all results along with calculation of individual risk through an online questionnaire.
Measures that can simply be obtained by questionnaires and without physical examination were the strongest predictors of all-cause mortality in the UK Biobank population. The prediction score we have developed accurately predicts 5 year all-cause mortality and can be used by individuals to improve health awareness, and by health professionals and organisations to identify high-risk individuals and guide public policy.
Knut and Alice Wallenberg Foundation and the Swedish Research Council.
This is one of the first report from the UK Biobank project including around 500,000 individual between 40-70 years followed up so far around 5 years. The participants provided health details through questionnaires, had a physical examination and gave bood and urine for biological measurements.
In this report the authors report on a Prediction Score for mortality derived from 13 self-reported predictors. In fact, all it shows is that if you ASK YOUR PATIENTS 4 SIMPLE QUESTIONS, you get most of the mortality prediction:
1. How old are you?...Age being the highest predictor of death...(surprise, surprise..!!!)
2. What gender?...men have a higher age-adjusted mortality than women...
3. Do you smoke? smoking is bad news...
4. Do you have difficulty walking?...if YES, thats bad news as you are not fit...
and thats it...
AGE + GENDER PREDICT ~70% of MORTALITY, the rest adds little!
Once more, that is the problem with mortality prediction scores: AGE+GENDER tells you most of what you need to know...
Lets hope the UK Biobank future results will prove more exciting...time will tell!
Rate of Change in Renal Function and Mortality in Elderly Treated Hypertensive Patients.
BACKGROUND AND OBJECTIVES:
Evidence relating the rate of change in renal function, measured as eGFR, after antihypertensive treatment in elderly patients to clinical outcome is sparse. This study characterized the rate of change in eGFR after commencement of antihypertensive treatment in an elderly population, the factors associated with eGFR rate change, and the rate's association with all-cause and cardiovascular mortality.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:
Data from the Second Australian National Blood Pressure study were used, where 6083 hypertensive participants aged ≥65 years were enrolled during 1995-1997 and followed for a median of 4.1 years (in-trial). Following the Second Australian National Blood Pressure study, participants were followed-up for a further median 6.9 years (post-trial). The annual rate of change in the eGFR was calculated in 4940 participants using creatinine measurements during the in-trial period and classified into quintiles (Q) on the basis of the following eGFR changes: rapid decline (Q1), decline (Q2), stable (Q3), increase (Q4), and rapid increase (Q5).
A rapid decline in eGFR in comparison with those with stable eGFRs during the in-trial period was associated with older age, living in a rural area, wider pulse pressure at baseline, receiving diuretic-based therapy, taking multiple antihypertensive drugs, and having blood pressure <140/90 mmHg during the study. However, a rapid increase in eGFR was observed in younger women and those with a higher cholesterol level. After adjustment for baseline and in-trial covariates, Cox-proportional hazard models showed a significantly greater risk for both all-cause (hazard ratio, 1.28; 95% confidence interval, 1.09 to 1.52; P=0.003) and cardiovascular (hazard ratio, 1.40; 95% confidence interval, 1.11 to 1.76; P=0.004) mortality in the rapid decline group compared with the stable group over a median of 7.2 years after the last eGFR measure. No significant association with mortality was observed for a rapid increase in eGFR.
In elderly persons with treated hypertension, a rapid decline in eGFR is associated with a higher risk of mortality.
There is something wrong with the world of publications and journals... So elderly patients with rapidly declining eGFR are more likely to die?!
And cjASN has a reasonable impact factor... !!!!!
We are drowning in information ... Most of it associative, a lot of it a rehash of previous work... And it means we can't see the wood from the trees ... The value of a publication now is primarily for the author rather than the wider readership...its like satellite TV ... Hundreds of channels but hardly anything worth watching!!!
Central arteriovenous anastomosis for the treatment of patients with uncontrolled hypertension (the ROX CONTROL HTN study): a randomised controlled trial.
Hypertension contributes to cardiovascular morbidity and mortality. We assessed the safety and efficacy of a central iliac arteriovenous anastomosis to alter the mechanical arterial properties and reduce blood pressure in patients with uncontrolled hypertension.
We enrolled patients in this open-label, multicentre, prospective, randomised, controlled trial between October, 2012, and April, 2014. Eligible patients had baseline office systolic blood pressure of 140 mm Hg or higher and average daytime ambulatory blood pressure of 135 mm Hg or higher systolic and 85 mm Hg or higher diastolic despite antihypertensive treatment. Patients were randomly allocated in a 1:1 ratio to undergo implantation of an arteriovenous coupler device plus current pharmaceutical treatment or to maintain current treatment alone (control). The primary endpoint was mean change from baseline in office and 24 h ambulatory systolic blood pressure at 6 months. Analysis was by modified intention to treat (all patients remaining in follow-up at 6 months). This trial is registered with ClinicalTrials.gov, number NCT01642498.
83 (43%) of 195 patients screened were assigned arteriovenous coupler therapy (n=44) or normal care (n=39). Mean office systolic blood pressure reduced by 26·9 (SD 23·9) mm Hg in the arteriovenous coupler group (p<0·0001) and by 3·7 (21·2) mm Hg in the control group (p=0·31). Mean systolic 24 h ambulatory blood pressure reduced by 13·5 (18·8) mm Hg (p<0·0001) in arteriovenous coupler recipients and by 0·5 (15·8) mm Hg (p=0·86) in controls. Implantation of the arteriovenous coupler was associated with late ipsilateral venous stenosis in 12 (29%) of 42 patients and was treatable with venoplasty or stenting.
Arteriovenous anastomosis was associated with significantly reduced blood pressure and hypertensive complications. This approach might be a useful adjunctive therapy for patients with uncontrolled hypertension.
This pilot study pertains to treat resistant hypertension by the creation of an iliac AV shunt...
Whilst seemingly promising, it is another example of the BIG INDUSTRIAL MEDICAL COMPLEX intrusion into clinical practice; the use of a potentially harmful, not to say dangerous, interventions to treat patients who may not need it (those whose SBP is above 140mmHg, whilst their age if over 70....) or who may be controlled otherwise...by a 4th antihypertensive agent...or better compliance...25-30% of so called resistant hypertensives are non compliant:
The AV shunt intervention exposes patients to a number of serious complications such as DVT as well as potential ischemic lower limb changes...
It is also an example of the BIG INDUSTRIAL MEDICAL COMPLEX influence on publishers...the publication in the Lancet, a seemingly serious journal, of a pilot study with short and inadequate follow-up as well as devoid of control/sham intervention group not to mention compliance to medical checks... In other words, a pilot, proof of concept, study with a number of serious limitations...published in a top medical journal...?!
This intrusion of the INDUSTRIAL MEDICAL COMPLEX was already demonstrated in patients with "resistant" hypertension by the Renal Sympathetic Denervation (RDN) clinical trials, SIMPLICITY...mostly badly designed an uncontrolled until SIMPLICITY HTN 3 showed no benefit...
BUT...the MEDICAL INDUSTRIAL COMPLEX...doesnt rest its case but pursue and encourage the greed of interventionists amongst private physicians...who saw in such method a major source of unethical income...by all sorts of subgroup analyses and posthoc analyses claiming benefits...:
in Japan: http://www.ncbi.nlm.nih.gov/pubmed/26102846
In subgroups: http://www.ncbi.nlm.nih.gov/pubmed/24914028
Younger patients: http://www.ncbi.nlm.nih.gov/pubmed/25565369
Number of bursts...
In other words, the MEDICAL INDUSTRIAL COMPLEX feeds on:
1. Pseudo clinical indications
2. Poorly managed patients, by conventional means
3. Credulous physicians who think any new technology is an advance...
4. Greedy physicians who make money out of new interventions at the expense of their patients' safety or benefit...in countries where private medicine thrives...
5. Medical Journals attracted by medical technical innovations...even when poorly designed, or pilot, studies underpin the findings...
IT IS HIGH TIME WE, AS A PROFESSION, PUT PATIENTS BENEFIT AND SAFETY BEFORE GADGETRY AND PROFIT...
Is There a Real Global Epidemic of Chronic Kidney Disease?
Numerous publications have asserted that the global prevalence of chronic kidney disease (CKD) in adults is generally between 10-13% (as determined from the KDOQI or KDIGO Classification schema, but using one-off, non-age calibrated determinations for identification of CKD ) and that the burden of this disease has reached “epidemic” proportions. In some developed countries (e.g. USA) the population-based prevalence rate of CKD has levelled off, at least in most adult age groups, and some countries have a much lower prevalence of CKD (e.g. Italy) than the global averages. A new and monumental study has put a fresh perspective to the issue of the global burden of CKD (Global Burden of Disease Study 2013 Collaborators, The Lancet, June 8, 2015 – on-line). This seminal study of the incidence, prevalence and years lived with disability (YLD) for 301 acute and chronic diseases (including CKD) and injuries in 188 countries during 1990 and 2013 sheds new light on the purported “epidemic” CKD. The data (35,620 distinct sources) were derived and analyzed in a fashion different from those publications using KDOQI or KDIGO criteria so they may not be strictly comparable. The inclusion of both adults and children may have also altered the prevalence data compared to KDOQI and KDIGO, which are confined to adults only.
Nevertheless the observations are quite informative. There were 324,666,000 cases of CKD in 1990 and 471,916,000 cases of CKD in 2013; after adjusted for aging and population growth the prevalence rate of CKD (per 100,000 population) actually declined overall by about 5% between 1990 and 2013. But the change in adjusted global prevalence rate between 1990- and 2013 was not uniform among the causes of CKD; to wit, the adjusted global prevalence rates of CKD due to glomerulonephritis and hypertension declined by 13.54% and 10.74% respectively whilst the adjusted global prevalence rates of CKD due to diabetes or other causes increased by 11.85% and 3.12% respectively. If the global population was 7.1 Billion in 2013 about 6.7% had some form of CKD; about 20% of which could be attributed to diabetes. The inclusion of children in both the denominator and numerator in this analysis may have diluted the overall prevalence rates of CKD, to some degee. But taken at face value, these figures indicate that generic CKD as a whole is not occurring in “epidemic” proportions globally, but that there are very worrisome trends over the last 2 decades in that CKD due to diabetes is a major and growing global problem. Correspondingly, the reported age and population standardized YLD rose by 10.6% and 6.9% for CKD due to Diabetes and other causes respectively between 1990 and 2013 whilst the age and population YLD fell 22.4% and 6.9% for CKD due to hypertension and glomerulonephritis respectively for a net decline in the YLD burden of CKD on a global basis.
Translating these intriguing findings into an action plan for control of the global disease burden linked to CKD is a difficult task and undoubtedly the answers will be different for developing compared to developed nations and depend greatly on the importance of CKD relative to other public health priorities (e.g. electrification, potable water, infectious disease, etc). What does seem abundantly clear, at least to me, is that the focus should not be on generic CKD, but rather on the problem of diabetes and its parent obesity. In my opinion, what the globe urgently needs is a coherent, culture-adapted approach to detection, prevention and management of obesity and diabetes (“diabesity”)—and not a population- based early detection program for generic CKD. Furthermore, more research leading to better understanding and treatments for the complex triad of obesity, diabetes and CKD are greatly needed. We should recognize that a global epidemic of generic CKD simply does not exist and relentlessly devote our energy to mitigating the world-wide problem of too many calories of the wrong kind and lack of energy consuming activities so as to avoid the CKD complications of “diabesity”.
Richard J. Glassock, MD
Geffen School of Medicine at UCLA
June 8, 2015
Prof Richard Glassock wrote in reference to the latest publication in the Lancet on the Global Burden of Disease Study 2013: (The Lancet On line 8th of June 2015)
It represents massive data collection and a complicated analysis but the main message is that except for diabetes related CKD, most forms of CKD are decreasing (since 1990) in total prevalence and years lost to disability.
The only "epidemic" of CKD is that related to diabetes, and indirectly to obesity.
The public health authorities around the world should not be focusing on detection of CKD, per se, as a problem, but instead should be energetically trying to curtail diabetes, by focusing on its origins; diet (composition and energy content) and activity level.
Claims that the world is trapped in an out-of-control epidemic of CKD represent mis-information at its worst, as these claims obfuscate the real issue; diabetes and its micro- and macro-vascular complications.
Screening programs for CKD are socially irresponsible, if they detract from addressing the real problem- diabesity (diabetes due to obesity), a potentially preventable disorder-- easily detected but difficult to treat.
Food for thought!!!
The global "epidemic" of CKD has been an ill founded concept based on very poor epidemiology and/or rather poor biostatistics.
This had a number of consequences, that I condemn:
1. Raised awareness of CKD, but overinflated its scale...claiming to affect 1 in 2 individual over a lifetime…
2. Medicalised the ageing process, by falsely claiming that CKD affected millions over the age of 65...thus confusing true CKD with age-related decline in kidney function…
3. Generated an industry of lightweight biostatistical analyses based on poorly collected and seldom validated data…published as irrefutable facts…
4. Raised the profile of Nephrology as a subspeciality, but at the price of misinformation...or to be kind, an unfounded truth...
5. Increased “Nephrologists” income in countries where their income stems from recognising, diagnosing, and cashing on, false diseases in an alarmed and misinformed population…
6. Failed to distinguish true CKD from community based older individuals with reduced kidney function…
7. Overburdened Nephrologists worldwide by unnecessary referrals of older patients with mild to moderate, but stable, age-related impaired kidney function; thus distracting them from their true task of dealing with primary and progressive nephropathies!
8. Increased prescription of potentially nephrotoxic agents such as ACE inhibitors in the elderly without a shred of evidence that it protected from early CKD progression or delayed ESRD, and in spite of evidence to the contrary:
9. Generated more diseases, namely AKI, in elderly individuals prescribed ACE inhibitors for dubious and ill founded indications…:
10. Overlooked the true burden of disease; namely Hypertension and Diabetes, thus leaving them significantly under-diagnosed and under-treated!
Shame on us as a professional body to have jumped uncritically on this bandwagon…
”Castles built on sand, soon collapse…”