Pesticides Found in Your Food Linked to Diabetes, Liver, Kidney and Brain Disease


Pesticides Found in Your Food Linked to Diabetes, Liver, Kidney and Brain Disease

 Long-term exposure to pesticides has been linked to infertility, birth defects, endocrine disruption, neurological disorders and cancer, so it’s a common-sense conclusion that fewer pesticides in our food supply would result in improved health among the general population.

In fact, one of the strongest selling points for eating organic food is that it can significantly lower your exposure to pesticides and other harmful chemicals used in conventional agriculture, and this measure in and of itself may help protect your long-term health and/or improve any health conditions you may have.

Since organic standards prohibit the use of synthetic pesticides and herbicides, organic foods are, as a rule, less contaminated, and studies have confirmed that those who eat a primarily organic diet have fewer toxins in their system.

Sadly, the chemical technology industry wields great power — so great that our government has largely turned a blind eye to the obvious, which is that too many toxic chemicals, in too great amounts, are being allowed in the growing of food. As noted in the featured film, “From DDT to Glyphosate:”

“Just as was the case in the 1950s with DDT and tobacco, we are on the brink of disastrous damage to health worldwide. This short film begins to explain why, and what we can do.”

Help Educate Those You Love

“From DDT to Glyphosate” is just half an hour long, yet it’s an excellent introduction to the dangers of pesticides.

The ‘Silent Spring’ Continues

In 1962, American biologist Rachel Carson wrote the groundbreaking book “Silent Spring,” in which she warned of the devastating environmental impacts of DDT (dichloro-diphenyl-trichloroethane), suggesting the chemical may also have harmful effects on human health.

She rightfully questioned the logic and sanity of using such vast amounts of a chemical without knowing much about its ecological and human health impact.

Her book triggered a revolution in thinking that gave birth to the modern environmental movement, and the public outcry that resulted from her book eventually led to DDT being banned for agricultural use in the U.S. in 1972.

Unfortunately, DDT was simply replaced with other equally unsafe and untested chemicals. Today, we’re also exposed to even vaster amounts of pesticides, and a wider variety of them, which is why it’s so important to share the above film with as many people as possible.

Consider this: the very same companies that developed chemical warfare weapons during World War II simply transitioned into agriculture after the war, and many of the same warfare chemicals are now sprayed on our food.

The notion that these chemicals are good for humans, the environment and the business of agriculture is a fabricated one.

Genetic Engineering Fuels the Chemical Agriculture Engine

As noted in the film, 80 percent of genetically engineered (GE) crops are designed to withstand herbicide application; most often glyphosate-based herbicides, such as Monsanto’s Roundup. As a result, we’re ingesting far greater quantities of pesticides than ever before.

The question is, where’s the breaking point? There’s reason to believe we may have crossed the threshold already. Health statistics suggest the average toxic burden has become too great for children and adults alike, and toxins in our food appear to play a primary role.

According to Dr. Joseph E. Pizzorno, founding president of Bastyr University, the first fully accredited multidisciplinary university of natural medicine and the first National Institutes of Health-funded center for alternative medicine research, toxins in the modern food supply are now “a major contributor to, and in some cases the cause of, virtually all chronic diseases.”

Watch the video. URL:https://youtu.be/mF2iS5vIamg

Kidney has a circadian clock that controls all metabolic process.


You sure didn’t know this. Kidneys have an internal clock which plays an important role in maintaining balance within the body, a new study has found.

Many of the body’s processes follow a natural daily rhythm or circadian clock that is based on regular light-dark cycles as the Earth rotates. Now, researchers have demonstrated that the kidney possesses such an intrinsic circadian clock that regulates and coordinates a variety of the organ’s functions.

“Since urine formation and excretion by the kidney is one of the most easily detectable rhythmic processes (we are forming and excreting much more urine during the day), we hypothesised that at least a part of this rhythmicity is dependent on the circadian clock mechanism,” said Natsuko Tokonami from University of Lausanne in Switzerland.

By blocking kidney cells’ expression of a gene that is critically involved in the circadian clock system, researchers found that the clock is responsible for the temporal adaptation of kidney function to the light and dark phases of the day that correspond to activity and rest.

Such adaptations have an important effect on the levels of various amino acids, lipids, and other components of blood in the body, researchers said. Furthermore, in individuals who take medications, the kidney’s circadian clock controls the process of drug elimination from the body and therefore can influence the duration of a drug’s action and the effectiveness of the therapy, they said.

“We have shown that the circadian clock in the kidney plays an important role in different metabolic and homeostatic processes at both the intra-renal and systemic levels and is involved in drug disposition,” said Dmitri Firsov from University of Lausanne. The findings were published in the Journal of the American Society of Nephrology (JASN).

Reduced Kidney Function Linked With Higher Risk Of Kidney And Urothelial Cancers.


Individuals with poor kidney function may require more intensive screening for these cancer types

Reduced kidney function may increase the risk of developing kidney and urothelial cancers, according to a study appearing in an upcoming issue of the Journal of the American Society of Nephrology (JASN). The findings suggest that patients with kidney disease may benefit from more intensive screenings for these types of cancer.

Chronic kidney disease and cancer are both major and growing public health problems. “While multiple studies have observed higher risks of cancer in persons with end-stage renal disease, the association of less severe kidney disease with cancer remains poorly understood,” said Alan Go, MD (Kaiser Permanente Northern California).

To investigate, Dr. Go and his colleagues analyzed information from nearly 1.2 million adult members of Kaiser Permanente in Northern California who were at least 40 years of age and who had no history of cancer, dialysis, or kidney transplantation. Kidney function was measured by estimated glomerular filtration rate (eGFR), with normal kidney function being over 60 ml/min/1.73m2 and kidney failure being below 15 ml/min/1.73m2.

During more than 6 million person-years of follow-up, 72,875 individuals developed cancer. (A person-year is the number of years of follow-up multiplied by the number of people in the study.) Among the major findings during follow-up:

Individuals with an eGFR of 45 to 59 had a 39% increased risk of kidney cancer (or renal cell carcinoma).
Individuals with an eGFR of 30 to 44 had an 81% increased risk of kidney cancer.
Individuals with an eGFR below 30 had a 100% (or a 2-fold) increased risk of kidney cancer.
Individuals with an eGFR below 30 had a 48% increased risk of urothelial cancer, which includes tumors in the bladder and ureters.
There were no significant links between eGFR and other cancer types such as prostate, breast, lung, and colorectal cancers.

The researchers noted that various biologic mechanisms may help to explain the links observed in this study. For example, kidney dysfunction causes a state of chronic inflammation and oxidative stress. “These and other mechanisms deserve further study in order to better define the link between kidney function and site-specific cancer risk,” said lead author Will Lowrance, MD, MPH (University of Utah).

In an accompanying editorial, Jonathan Hofmann, PhD and Mark Purdue, PhD (National Cancer Institute) noted that the study is “an important step forward in characterizing the relationship between chronic kidney disease and risk of renal cell carcinoma and other malignancies. Studies such as this further support an etiologic role of impaired renal function in the development of renal cell carcinoma.”

 

Source: American Society of Nephrology

 

Research findings point to new therapeutic approach for common cause of kidney failure.


New research has uncovered a process that is defective in patients with autosomal dominant polycystic kidney disease, a common cause of kidney failure. The findings, which appear in an upcoming issue of the Journal of the American Society of Nephrology (JASN), point to a new potential strategy for preventing and treating the disease.

Polycystic kidney disease (PKD), the fourth leading cause of kidney failure worldwide, comes in two forms: autosomal dominant polycystic kidney disease (ADPKD) develops in adulthood and is quite common, while autosomal recessive polycystic kidney disease (ARPKD) is rare but frequently fatal. ADPKD is caused by mutations in either of two proteins, polycystin-1 and polycystin-2, while ARPKD is caused by mutations in a protein called fibrocystin. There is no cure or widely adopted clinical therapy for either form of the disease.

Polycystin-1, polycystin-2, and fibrocystin are all found in a cell’s primary cilium, which acts as the cell’s antenna and is intimately involved in human embryonic development as well as the development of certain diseases, including PKD. “What we don’t know, and were hoping to better understand, is what goes wrong with these proteins in the cells of PKD patients and what kinds of therapies might help those cells,” said Joseph Bonventre, MD, PhD (Brigham and Women’s Hospital).

Dr. Bonventre and his colleagues Benjamin Freedman, PhD and Albert Lam, MD led a team of scientists at Brigham and Women’s Hospital, the Mayo Clinic, and the Harvard Stem Cell Institute as they studied cells obtained from five PKD patients: three with ADPKD and two with ARPKD. The investigators reprogrammed patients’ skin cells into induced pluripotent stem cells, which can give rise to many different cell types and tissues. When the researchers examined these cells under the microscope, they discovered that the polycystin-2 protein traveled normally to the antenna, or cilium, in cells from ARPKD patients, but it had trouble reaching the antenna in ADPKD patients. When they sequenced the DNA in these ADPKD patient cells, the investigators found mutations in the gene that encodes polycystin-1, suggesting that polycystin-1 helps shepherd polycystin-2 to the cilium.

“When we added back a healthy form of polycystin-1 to our patient cells, it traveled to thecilium and brought its partner polycystin-2 with it, suggesting a possible therapeutic approach for PKD,” explained Dr. Freedman. “This was the first time induced pluripotent stem cells have been used to study human kidney disease where a defect related to disease mechanisms has been found.”

The researchers noted that reprogrammed stem cells from patients with ADPKD may also be useful for testing new therapeutics before trying them out in humans.

In an accompanying editorial, Alexis Hofherr, MD and Michael Köttgen, MD (University Medical Centre, in Freiburg, Germany) stated that the study has “laid the groundwork for using induced pluripotent stem cells in PKD research. This important step forward will provide novel opportunities to model PKD pathogenesis with human cells with defined patient mutations.”

 

 

Scientists generate “mini-kidney” structures from human stem cells.


Diseases affecting the kidneys represent a major and unsolved health issue worldwide. The kidneys rarely recover function once they are damaged by disease, highlighting the urgent need for better knowledge of kidney development and physiology.

Now, a team of researchers led by scientists at the Salk Institute for Biological Studies has developed a novel platform to study  diseases, opening new avenues for the future application of regenerative medicine strategies to help restore kidney function.

Salk scientists generate “mini-kidney” structures from human stem cells

For the first time, the Salk researchers have generated three-dimensional kidney structures from human stem cells, opening new avenues for studying the development and diseases of the kidneys and to the discovery of new drugs that target human . The findings were reported November 17 in Nature Cell Biology.

Scientists had created precursors of kidney cells using stem cells as recently as this past summer, but the Salk team was the first to coax human stem cells into forming three-dimensional cellular structures similar to those found in our kidneys.

“Attempts to differentiate human stem cells into renal cells have had limited success,” says senior study author Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and holder of the Roger Guillemin Chair. “We have developed a simple and efficient method that allows for the differentiation of human stem cells into well-organized 3D structures of the ureteric bud (UB), which later develops into the collecting duct system.”

The Salk findings demonstrate for the first time that pluripotent stem cells (PSCs)—cells capable of differentiating into the many cells and tissue types that make up the body—can made to develop into cells similar to those found in the ureteric bud, an early developmental structure of the kidneys, and then be further differentiated into three-dimensional structures in organ cultures. UB cells form the early stages of the human urinary and reproductive organs during development and later develop into a conduit for urine drainage from the kidneys. The scientists accomplished this with both human  and induced  (iPSCs),  from the skin that have been reprogrammed into their pluripotent state.

After generating iPSCs that demonstrated pluripotent properties and were able to differentiate into mesoderm, a germ cell layer from which the kidneys develop, the researchers made use of growth factors known to be essential during the natural development of our kidneys for the culturing of both iPSCs and embryonic stem cells. The combination of signals from these growth factors, molecules that guide the differentiation of stem cells into specific tissues, was sufficient to commit the cells toward progenitors that exhibit clear characteristics of renal cells in only four days.

The researchers then guided these cells to further differentiated into organ structures similar to those found in the ureteric bud by culturing them with kidney cells from mice. This demonstrated that the mouse cells were able to provide the appropriate developmental cues to allow human  to form three-dimensional structures of the kidney.

In addition, Izpisua Belmonte’s team tested their protocol on iPSCs from a patient clinically diagnosed with polycystic  (PKD), a genetic disorder characterized by multiple, fluid-filled cysts that can lead to decreased  and kidney failure. They found that their methodology could produce kidney structures from patient-derived iPSCs.

Because of the many clinical manifestations of the disease, neither gene- nor antibody-based therapies are realistic approaches for treating PKD. The Salk team’s technique might help circumvent this obstacle and provide a reliable platform for pharmaceutical companies and other investigators studying drug-based therapeutics for PKD and other kidney diseases.

“Our differentiation strategies represent the cornerstone of disease modeling and drug discovery studies,” says lead study author Ignacio Sancho-Martinez, a research associate in Izpisua Belmonte’s laboratory. “Our observations will help guide future studies on the precise cellular implications that PKD might play in the context of .”

CKD: Lower Salt Intake May Reduce Heart Risks.


A diet with restricted salt intake may help to reduce the risk for cardiovascular disease in patients with chronic kidney disease (CKD), as well as the risk for CKD progression, according to an article published online November 7 in the Journal of the American Society of Nephrology.

Emma J. McMahon, PhD candidate, University of Queensland, Australia, and colleagues conducted a double-blind, placebo-controlled randomized crossover trial involving 20 adult patients with stage 3 to 4 CKD. In the phase I portion of the LowSALT CKD study, the researchers evaluated the effects of high vs low sodium intake on several physiological measures, including ambulatory blood pressure, protein excretion, and body fluid status.

The researchers counseled patients to eat a low-sodium (1080 – 1440 mg/day) diet during the 1-week run-in period of the 6-week study, they then randomly assigned patients to either a high-sodium or low-sodium diet. Those on the high-sodium diet had a goal of 1080 to 1440 mg/day plus 2160 mg/day from a slow-release tablet. Those on the low-sodium diet had a goal of 1080 to 1440 mg/day plus a placebo capsule. Patients crossed over after an intermediate washout week.

The investigators found a mean reduction of 9.7/3.9 mm Hg in blood pressure in patients on the low-salt diet compared with the high-salt diet. The reductions were consistent during a 24-hour period with no significant difference between daytime and nighttime measurements. Researchers also found that patients had reductions in fluid volume, body weight, and protein in the urine while on the low-salt diet.

“If these findings are transferable to the larger CKD population and shown to be sustainable long-term, this could translate to markedly reduced risk of cardiovascular events and progression to end-stage kidney disease, and it could generate considerable health-care savings,” senior author Katrina J. Campbell, PhD, from Princess Alexandra Hospital, Queensland, said in a news release.

“These are clinically significant findings, with this magnitude of blood pressure reduction being comparable to that expected with the addition of an anti-hypertensive medication and larger than effects usually seen with sodium restriction in people without CKD,” McMahon noted in the release. “If maintained long-term, this could reduce risk of progression to end-stage kidney disease — where dialysis or transplant is required to survive — by 30%.”

“This study is salient because few intervention studies have evaluated dietary sodium reduction in patients with CKD, write Cheryl A.M. Anderson, PhD, MPH, and Joachim H. Ix, MD, both from the University of California San Diego School of Medicine, in an accompanying editorial. “The evaluation of other outcomes in addition to BP is an additional strength of the trial.”

Intrarenal Resistive Index after Renal Transplantation.


BACKGROUND

The intrarenal resistive index is routinely measured in many renaltransplantation centers for assessment of renal-allograft status, although the value of the resistive index remains unclear.

METHODS

In a single-center, prospective study involving 321 renal-allograft recipients, we measured the resistive index at baseline, at the time of protocol-specified renal-allograft biopsies (3, 12, and 24 months after transplantation), and at the time of biopsies performed because of graft dysfunction. A total of 1124 renal-allograft resistive-index measurements were included in the analysis. All patients were followed for at least 4.5 years after transplantation.

RESULTS

Allograft recipients with a resistive index of at least 0.80 had higher mortality than those with a resistive index of less than 0.80 at 3, 12, and 24 months after transplantation (hazard ratio, 5.20 [95% confidence interval {CI}, 2.14 to 12.64; P<0.001]; 3.46 [95% CI, 1.39 to 8.56; P=0.007]; and 4.12 [95% CI, 1.26 to 13.45; P=0.02], respectively). The need for dialysis did not differ significantly between patients with a resistive index of at least 0.80 and those with a resistive index of less than 0.80 at 3, 12, and 24 months after transplantation (hazard ratio, 1.95 [95% CI, 0.39 to 9.82; P=0.42]; 0.44 [95% CI, 0.05 to 3.72; P=0.45]; and 1.34 [95% CI, 0.20 to 8.82; P=0.76], respectively). At protocol-specified biopsy time points, the resistive index was not associated with renal-allograft histologic features. Older recipient age was the strongest determinant of a higher resistive index (P<0.001). At the time of biopsies performed because of graft dysfunction, antibody-mediated rejection or acute tubular necrosis, as compared with normal biopsy results, was associated with a higher resistive index (0.87±0.12 vs. 0.78±0.14 [P=0.05], and 0.86±0.09 vs. 0.78±0.14 [P=0.007], respectively).

CONCLUSIONS

The resistive index, routinely measured at predefined time points after transplantation, reflects characteristics of the recipient but not those of the graft.

 

Souirce: NEJM

 

 

Chronic kidney failure no barrier to CT angiography.


CT angiography (CTA) using moderate doses of IV contrast in patients with advanced renal failure is a safe procedure that negatively affects renal function in only a small percentage of patients, according to researchers from Baltimore.

But the imaging options are even better with newer MDCT scanners. CTA protocols with low kVp and using half the normal dose of iodinated contrast have even less impact on kidney patients and produce excellent images, said Dr. Barry Daly from the University of Maryland.

In a study presented at last month’s International Society for Computed Tomography (ISCT) meeting in San Francisco, Daly showed how even normal contrast doses had little effect on serum creatinine levels in most patients. Information gained by the studies far outweighs the chance of adverse effects in patients with chronic renal failure, he said.

Daly also showed his latest protocol for low-contrast-dose, low-kV CTA imaging that delivers high image quality with even less risk for these patients.

Don’t skip the CTA

CTA isn’t something you want to skip, even though many centers do just that, he said. Before renal transplant surgery, for example, surgeons need to see what they’re going to be dealing with in the operating room.

“There are big risks going into surgery without CTA in this group because they have the risk of a major change in operative procedure, prolonged surgery, poor graft outcomes, failure to engraft, loss of the organ — which is a total disaster, especially in the setting of matched renal donor transplantation — and, of course, the possibility of missing important pathologies,” Daly said.

Incidental right iliac venous stent
Patient is in renal failure but not yet on dialysis. CTA was acquired at 80 kVp and 360 mAs following administration of 50 mL of 350 mg/mL contrast. Contrast density in the iliac arteries is > 400 HU. Radiation dose is 4.3 mSv. There is an incidental right iliac venous stent. Images courtesy of Dr. Barry Daly.

Daly and colleagues reviewed the use of CTA in 180 potential renal transplant recipients, all with matched donors, “but we were especially interested in looking at a predialysis cohort of 40 patients,” he said.

Patients were assessed for aortoiliac and calcific atherosclerosis, venous thrombosis, and increased incidence of renal cell carcinoma (four to seven times the normal rate in native kidneys). The only prophylaxis was aggressive oral hydration both before and after CTA, he said.

It’s important to find an appropriate place for the engraftment, Daly said. Many patients may require surgical correction with bypass grafts before transplantation can be done.

“Because a lot of these folks have had chronic hemodialysis, it’s not uncommon to find occlusion of the iliac veins,” he said. In a couple of cases, this has become obvious only in the operating room — “with disastrous consequences.”

The study measured serum creatinine (SeCr) and estimated glomerular filtration rate (eGFR) before and after imaging in the 40 predialysis patients. “There was almost no difference between the two groups in mean measurements,” Daly said.

“Nobody had to undergo dialysis, but looking at the changes, there clearly were some shifts that we shouldn’t ignore,” he said.

Post CTA, 27 patients had stable or mean decreased SeCr of 10.2%. Thirteen patients had a mean increase of 6.3%, with one patient showing a 32% rise, and three saw almost no change (0.5-1.5 mg/dL increase).

Change in SeCr after CTA in predialysis cohort of 40 patients

SeCr mean SeCr range eGFR mean
Pre-CTA 5.2 2.9-14.1 20.5
Post-CTA 5.1 2.4-14.2 21.0

A low rate of contrast-induced nephropathy (CIN) in renal patients isn’t all that surprising, Daly said. Newhouse, Katzberg, and others have shown that the risks of IV low-osmolar contrast precipitating CIN have been overestimated.

These previous studies demonstrate that moderate doses of IV contrast are much less nephrotoxic than arterial administration, he said. Many studies without controls failed to allow for other factors affecting renal function, especially in hospital populations. Finally, a 2010 study in Radiologyshowed that low-osmolar contrast may be as safe as iso-osmolar contrast, he noted.

Low-kVp, low-contrast-dose CTA

Daly and colleagues also performed a study of low-kVp, low-contrast-dose CTA in chronic renal failure patients. Why is this necessary if the regular dose is safe?

“The answer, of course, is that lower is always better,” Daly said. Even if the negative effects aren’t as bad as they were feared to be, “there is still a small portion of patients in our group who are still at risk with the conventional dose,” he said, adding that “new CT scanners have enabled new techniques for getting more out of each gram of iodine.”

The technique involves dropping the kV and increasing the mAs. For example, if you drop the tube current from 120 kV to 80 kV, you would increase the mAs by a factor of 2.7. Thus, 120 kVp and 250 mAs become 80 kV and 600 mAs, he said, and for large patients the tube may reach the maximum mAs.

MDCT can be used with extended z-axis coverage to shorten scan times to correspond to a shorter bolus train. Ideally, there should be at least 40 mm to 80 mm of coverage, he advised.

How it works is by now well-known, he said. “The k-edge of iodine is only [33.2] keV, so by dropping our kVp we can actually get considerably increased x-ray absorption. There’s a nearly a twofold increase in iodine attenuation at 80 kV compared to 120 kV.” Thus, the iodine dose can be cut in half while producing similar CT values, according to Daly.

The researchers perform the 80-kV studies on a Brilliance iCT 256 or a Brilliance 64 scanner (Philips Healthcare) using 320 to 350 mgI/mL of contrast.

They inject 35 to 50 mL of contrast at 4 mL per second in a peripheral vein, followed by 40 to 60 mL of a saline chaser at 4 mL per second. Automated bolus tracking is set for a 120- to 150-HU threshold in the aorta just below the hiatus, and the automated minimum scan delay is set to 4.2 to 6.5 seconds, he said.

Tube rotation speed is 0.75 seconds for a 256-slice scanner and 0.75 to 1 second for a 64-detector-row scanner. mAs values are based on patient body mass index (noise present at precontrast phase) with pitch set at maximum for the mAs selected, Daly said.

The resulting images look great, but using iterative reconstruction (iDose5, Philips) allows even lower doses, or the scanning of larger patients using low-kV, low-contrast protocols, he said.

In summary, CTA with a moderate 100-mL dose of iso-osmolar contrast in advanced renal failure “is a safe procedure with a negative impact on renal function in only a small percentage of patients,” Daly said, adding that “these aren’t patients with creatinine of 1.8, these are patients with major renal compromise.”

However, even though the 100-mL contrast protocol has a “very limited negative effect on people … a better option today is low 80-kVp, low-contrast-dose CTA technique with 35 to 50 mL of iso-osmolar contrast,” Daly said.

This very safe technique yields high diagnostic quality and works on most newer CT scanners, he added.

“Finally, if you have the benefit of iterative reconstruction, it improves image quality and allows us to use this technique even in very large patients,” Daly said.

Hydration before contrast cuts CIN in high-risk patients.


Even patients with advanced kidney disease can steer clear of contrast-induced nephropathy (CIN) if given plenty of hydration, say researchers from the Netherlands. Results from the study of nearly 1,000 patients with stage 3 or 4 kidney disease were published in the June issue of Radiology.

The study found that fewer than 2.5% of the patients examined developed CIN when current guidelines emphasizing hydration were followed, according to the researchers from Radboud University Nijmegen Medical Centre in the Netherlands. The study also found that heart failure, low body mass index, and repeat contrast administration were associated with CIN.

CIN is the third most common cause of acute renal failure in hospitalized patients, and while most cases are limited to mild and transient impairment of renal function, serious morbidity and mortality, as well as longer hospital stays, can occur.

“In current practice, hydration is considered the preventive method of choice; however, evidence supporting its use is limited,” wrote Dr. Corinne Balemans and colleagues. Previous studies have relied on a variety of hydration protocols that were often used inconsistently (Radiology, June 2012, Vol. 263:3 pp. 706-713).

Balemans and colleagues aimed to determine risk factors associated with CIN by evaluating its incidence in patients with an estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m2 who received iodinated contrast media intravenously and were treated using current guidelines.

Current CIN guidelines developed in Europe and the U.S. emphasize the identification of patients at high risk for CIN and the use of hydration as a preventive measure, either using normal saline or sodium bicarbonate as an alternative option, they wrote.

In the study, patients with renal insufficiency were evaluated at a special outpatient clinic where CIN was assessed and normal saline hydration was prescribed (Centraal Begeleidings Orgaan guidelines, 2007), with renal function assessed after the procedures.

The researchers stratified all patients with eGFR less than 60 mL/min/1.73 m2 for risk of CIN; those at high risk based on absolute GFR and risk factors were hydrated with 1,000 mL of isotonic saline before and after contrast injection. Serum creatinine was measured three to five days later, and CIN was defined as an increase of 25% or more from baseline. Finally, the authors recorded and compared risk factors between patients with CIN and those without using stepwise multiple logistic regression analysis.

The study included 747 patients (43% female; mean age, 71.3 years ± 10) who underwent 944 procedures. Patients were hydrated in 511 (54.1%) procedures. CIN developed after 23 procedures (2.4%).

Independent predictors of CIN were heart failure (odds ratio, 3.0), body mass index (BMI) (odds ratio, 0.9), and repeated contrast material administration (odds ratio, 2.8), Balemans and colleagues wrote. No patients needed dialysis.

The population was carefully prepared before iodinated contrast injection, and only 7.7% of patients at high risk for CIN did not receive hydration.

“Our study provides reliable estimates of CIN and shows that the incidence of CIN is low in a homogeneous population of patients with stage 3 or 4 chronic kidney disease who underwent treatment in accordance with existing guidelines and who received intravenous iodinated contrast material,” the authors wrote.

In the study, money was saved by restricting hydration to about half of the study population; patients at high risk for CIN were hydrated, whereas those at low risk were not. However, it’s possible the incidence could have been reduced further by a less restrictive policy.

Regarding heart failure, a well-known risk factor for CIN, such patients may have more severe atherosclerotic vascular disease and are more prone to hemodynamic changes during and after procedures. For them, hydration may not be helpful, the authors wrote.

The inverse association between BMI and CIN may not have been reported previously, they noted. Patients with low BMI usually have a lower percentage of muscle mass, and as a result the formulas used to calculate eGFR overestimate renal function, Balemans and colleagues wrote.

Another study reported the association between repeat contrast exposure and CIN. In that study (Trivedi and Foley), the increased risk was even notable in patients with preserved renal function.

As for study limitations, the population was large but the number of events was small. Absolute GFR was used to classify risk, and there is debate about whether GFR should be corrected for body surface area.

The incidence of CIN in patients with stage 3 or 4 chronic kidney disease is low when treated in accordance with current guidelines, the authors concluded.

“Our findings support the efficacy of hydration regimens,” they wrote. “The risk of CIN is increased in patients with heart failure, low BMI, and repeated contrast material administration. These risk factors need to be validated in future studies.”

Decline in 20-year mortality after myocardial infarction in patients with chronic kidney disease: evolution from the prethrombolysis to the percutaneous coronary intervention era.


Cardiovascular disease is the main cause of death in patients with chronic kidney disease (CKD). Here we measured temporal trends in treatment and mortality after myocardial infarction (MI) depending on kidney function at presentation in 12,087 patients admitted for MI to a coronary care unit from 1985 to 2008. The patients were categorized into those with normal kidney function (estimated glomerular filtration rate over 90ml/min per 1.73m2), and those with CKD as defined by Kidney Foundation practice guidelines, with 8632 patients (71%) at CKD stages 2–5. Use of evidence-based care increased over time in all CKD stages. Mortality rates fell over the entire time period. When comparing data from 2000–2008 to that from 1985–1990, adjusted 30-day mortality fell both in patients with CKD stages 4–5 (adjusted odds 0.33, 95% confidence interval 0.18–0.60) and in those without kidney impairment (adjusted odds 0.21, 95% confidence interval 0.10–0.42). This mortality decrease was sustained during long-term follow-up. There was no significant interaction between kidney function and decade of admission. Overall, median survival was over 20, 15, 8, and 1.8 years for patients with normal kidney function, stage 2, stage 3, and stage 4–5 CKD, respectively. Thus, during the past 25 years, treatment of patients with a MI improved substantially with a concomitant decline in mortality. Although our findings were similar for all stages of kidney function, the prognosis remains poor for patients with stage 4–5 CKD.

Sourcardioe: Nature.