By Robert Preidt, HealthDay Reporter

THURSDAY, April 16, 2015 (HealthDay News) -- Genes may play a role in cardiac arrest risk among kidney patients who are on dialysis, new research suggests.

In a study of pairs of kidney patients who were on dialysis, the risk of cardiac arrest was 70 percent higher in the pairs where the two patients were blood relatives.

In general, patients on dialysis are 20 times more likely to suffer cardiac arrest than people in the general population, and cardiac arrest is the leading cause of death among patients on dialysis, the researchers noted.

The finding suggests that genes may play a role in cardiac arrest risk among these patients, and that pinpointing these genes may lead to new treatments to lower the risk, the researchers added.

The study was published online April 16 in the Journal of the American Society of Nephrology.

"These findings advance the science because they suggest that genetic factors -- or differences in DNA sequence -- contribute to the high risk of sudden death among patients on dialysis," study author Dr. Kevin Chan, from Massachusetts General Hospital in Boston, said in a journal news release.

"It paves the way for more detailed genetic studies in the dialysis population to find specific genes that could explain the high risk of cardiac arrest and potentially new treatments for these patients," he added.

The researchers analyzed data from nearly 650,000 dialysis patients, focusing on about 5,100 pairs of patients from the same family. Each patient was then matched to an unrelated control patient. Cardiac arrest was the cause of death in both patients in 4.3 percent of the family pairs, compared with 2.6 percent of unrelated pairs of patients.

Compared with unrelated pairs, the risk of dual cardiac arrest was 88 percent higher among genetically related family members who did not live together, and 66 percent higher among genetically related family members who did live together.

Dialysis patients who were spouses were not at increased risk for cardiac arrest.

More information

The National Kidney Foundation has more about dialysis.

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Nephrology follow-up of intensive care patients with acute kidney injury (AKI) requiring renal replacement therapy (RRT) rarely occurs, a new English study suggests. So researchers are proposing a protocol to encourage nephrologist visits to help protect patients from long-term renal dysfunction.

For the study, Christopher J. Kirwan, MD, of The Royal London Hospital, and colleagues reviewed the medical records of more than 5,500 intensive care patients at East London hospitals, including 219 who survived following continuous RRT for AKI; none were receiving renal care prior to hospitalization.

Just 26 patients (12%) saw a nephrologist for follow-up care after hospital discharge, according to results published in Nephron. (In the United Kingdom, a nephrologist isn't required to commence RRT in the ICU.) What's more, many had poor kidney function. At 3 to 6 months, the estimated glomerular filtration rate (eGFR) had fallen from baseline (48 vs. 60 mL/min/1.73 m²). The prevalence of chronic kidney disease stage 3 to 5 among patients also rose from 49% to 70%.

According to the researchers, a “higher eGFR at discharge should not be taken as universally reassuring.” Creatinine and eGFR levels can fluctuate for various reasons, and it is difficult to predict during hospitalization which patients will require nephrology follow-up.

The investigators proposed a pathway to shuttle appropriate ICU patients to nephrology follow-up:

•      If AKI is stage 2–3 during hospitalization, then measure creatinine at discharge. If the numbers are favorable, suggest follow-up at an AKI clinic within 3 months.
•      Early nephrology follow-up within 2–4 weeks after discharge should occur for patients with certain adverse features (i.e., significant increase in creatinine or renal impairment based on creatinine or eGFR.)
•      If renal function is stable, assess patient again after a year. If unstable, conduct regular follow-up.
•      Patients with the following features should be referred directly to specialist nephrology care after hospital discharge: persistent hematuria or proteinuria, glomerulonephritis, refractory hypertension, familial renal disease, extensive or recurrent nephrolithiasis, or likely progression to end-stage renal disease.

Source

1. Kirwan, C, et al. Nephron, 2015; doi: 10.1159/000371448.

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Among a group of more than 320,000 children, intrauterine exposure to gestational diabetes mellitus diagnosed by 26 weeks' gestation was associated with risk of autism spectrum disorders (ASDs), according to a study in the April 14 issue of JAMA. Maternal pre-existing type 2 diabetes was not significantly associated with risk of ASD in offspring.

Exposure of fetuses to maternal hyperglycemia may have long-lasting effects on organ development and function. Previous studies have revealed long-term risks of obesity and related metabolic disorders in offspring of women who had diabetes prior to pregnancy as well as women with hyperglycemia first detected during pregnancy. Whether such exposure can disrupt fetal brain development and heighten risk of neurobehavioral developmental disorders in offspring is less clear, according to background information in the article.

Anny H. Xiang, PhD, of Kaiser Permanente Southern California in Pasadena, Calif., and colleagues analyzed data from a single health care system to assess the association between maternal diabetes, both known prior to pregnancy and diagnosed during pregnancy, and the risk of ASD in children. The study included 322,323 children born from 1995-2009 at Kaiser Permanente Southern California (KPSC) hospitals. Children were tracked from birth until the first of the following: date of clinical diagnosis of ASD, last date of continuous KPSC health plan membership, death due to any cause, or Dec. 31, 2012.

Of the children included in the study, 6,496 (25) were exposed to pre-existing type 2 diabetes, 25,035 (7.8%) were exposed to GDM, and 290,792 (90.2%) were unexposed. Following birth (median of 5.5 years), 3,388 children were diagnosed as having ASD (115 exposed to pre-existing type 2 diabetes, 130 exposed to GDM at 26 weeks or less, 180 exposed to GDM at more than 26 weeks, and 2,963 unexposed). After adjustment for various factors, including maternal age, household income, race/ethnicity, and sex of the child, GDM diagnosed by 26 weeks was significantly associated with risk of ASD in offspring, but maternal pre-existing type 2 diabetes was not.

The increased ASD risk was independent of maternal smoking, prepregnancy body mass index, and gestational weight gain. Antidiabetic medication use was not independently associated with ASD risk in offspring.

The authors write that potential biological mechanisms linking intrauterine hyperglycemia and ASD risk in offspring may include multiple pathways, such as hypoxia (a lower-than-normal concentration of oxygen in the blood) in the fetus, oxidative stress in cord blood and placental tissue, chronic inflammation, and epigenetics (something that affects a cell, organ or individual without directly affecting its DNA).
 

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