No abstract

Rapid correction of chronic hyponatremia is known to cause demyelination syndromes, which are attributed to the rapid shift of water out of the brain. In uremic patients with hyponatremia, depending on the dialysate sodium concentration and delivered Kt/V, serum sodium levels may be rapidly corrected inadvertently during the hemodialysis (HD) session. It is not known whether uremic patients are as susceptible to the development of demyelination as patients with normal renal function. Since urea diffuses slowly across the blood-brain barrier, it can act as an effective osmole between plasma and the brain if levels are changed abruptly. During HD, blood urea levels drop suddenly and significantly and cerebral edema may develop (dialysis disequilibrium syndrome). This effect may counteract the fluid shift out of the brain during correction of hyponatremia. Therefore, theoretically, uremic patients may be less prone to develop demyelination. We present a patient with renal failure whose hyponatremia was corrected rapidly during HD to illustrate the potential problem. The patient tolerated rapid correction of hyponatremia without sustaining any neurologic damage. We performed a literature search looking for similar case reports and reviewed the scientific evidence behind the above hypothesis.

Genome-wide association studies have identified the cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1 (CDKAL1) gene as a novel risk factor for type 2 diabetes mellitus. Application of this genetic marker for prevention of type 2 diabetes and metabolic syndrome (MetS) in healthy populations has not yet been evaluated. The authors examined the effects of a CDKAL1 polymorphism (rs9465871) on metabolic phenotype and of gene-lifestyle (CDKAL1-energy intake) interaction on MetS in a cohort of apparently healthy Japanese men examined in 2003. The CC genotype of the CDKAL1 variant was associated with elevated glycosylated hemoglobin A₁(c) (HbA1c) levels. The prevalence of MetS was 25.6% for CC and 16.3% for TT + CT (odds ratio = 2.18, 95% confidence interval: 1.06, 4.48; P = 0.035). When dietary energy intake was accounted for, the variant's effect on HbA1c was observed in the highest energy-intake group (mean: CC, 5.6% (standard deviation, 1.7); TT + CT, 5.0% (standard deviation, 0.5); P = 0.025). In addition, the positive association between HbA1c and energy intake was stronger in subjects with the CC genotype than in subjects with TT + CT. These results suggest that the interaction between the CDKAL1 polymorphism and dietary energy intake influences the dysglycemic phenotype leading to MetS, possibly through impaired insulin secretion. The CDKAL1 polymorphism may be a marker for MetS in the Japanese population.

Reports of human immunodeficiency virus-associated nephropathy (HIVAN) occurring in Hispanics, females and heterosexuals are scarce. We reviewed 858 charts from our total HIV population to determine the prevalence and epidemiology of HIVAN at our center, and to evaluate the renal and patient survival among individual groups, according to race, sex and HIV risk factor. The prevalence of HIVAN was low (1.9%), relative to other centers (4–13%). Although Hispanics accounted for 56% of the HIV population, only 38% of HIVAN patients were Hispanic. The absolute risk of HIVAN in blacks was 3.6%, and in Hispanics was 1.3%. The relative risk of blacks vs. Hispanics was 2.8% (p < 0.04). Women and men were represented equally in both the HIVAN and HIV populations. The mean (± SE) rate of decline in glomerular filtration rate was 3.7 ± 0.9 ml/min/month, and patient survival following the onset of HIVAN was 23.6 ± 4.8 months. We found no difference in renal or patient survival between individual groups. In summary, the risk of HIVAN in Hispanics is similar to that for whites. Male sex is not an independent risk factor. Both renal and patient survival are similar in blacks and Hispanics, and in men compared to women.