Lee H, et al. J Korean Med Sci. 2014 Sep;29(Suppl 2):S91-S96. http://dx.doi.org/10.3346/jkms.2014.29.S2.S91

The number of elderly patients with end-stage renal disease is increasing rapidly. The higher prevalence of comorbidities and shorter life expectancy in these patients make it difficult to decide on the type of vascular access (VA). We explored the optimal choice for VA in elderly hemodialysis patients. We included elderly patients (> 65 years) visiting our VA clinic and divided them into three groups as follows: radiocephalic arteriovenous fistula (AVF), brachiocephalic AVF, and prosthetic arteriovenous graft (AVG). The primary outcomes were VA abandonment and all-cause mortality. The secondary outcome was maturation failure (MF). Of 529 patients, 61.2% were men. The mean age was 73.6 ± 6.0 years. The VA types were as follows: 49.9% radiocephalic AVF, 31.8% brachiocephalic AVF, and 18.3% AVG. Patients with an AVG tended to be older, female, and have a lower body mass index. More than half of patients (n = 302, 57.1%) started dialysis with central catheters, but the proportion of predialysis central catheter placement was not different among the VA types. Radiocephalic AVF was significantly superior to AVG in terms of VA abandonment (P = 0.005) and all-cause mortality (P < 0.001) in spite of a higher probability of MF. Brachiocephalic AVF was associated with a shorter time to the first needling and fewer interventions before maturation than radiocephalic AVF. Autologous AVF was suggested as the preferred VA choice in terms of long-term outcomes in elderly patients.

Shin TY, et al. Investig Clin Urol. 2020 Nov;61(6):555-564. https://doi.org/10.4111/icu.20200086

Although dysnatremia has been reported to be correlated with mortality risk, this issue remains unresolved in patients undergoing continuous renal replacement therapy (CRRT). Furthermore, it has not been determined whether change in or correction of sodium is related to mortality risk in this subset. A total of 569 patients were prospectively enrolled at the start of CRRT between May 2010 and September 2013. The patients were divided into 5 groups: normonatremia (135–145 mmol/L), mild hyponatremia (131.1–134.9 mmol/L), moderate to severe hyponatremia (115.4–131.0 mmol/L), mild hypernatremia (145.1–148.4 mmol/L), and moderate to severe hypernatremia (148.5–166.0 mmol/L). The non-linear relationship between sodium and mortality was initially explored. Subsequently, the odds ratios (ORs) for 30-day mortality were calculated after adjustment of multiple covariates. The relationship between baseline sodium and mortality was U-shaped. The mild hyponatremia, moderate to severe hyponatremia, and moderate to severe hypernatremia groups had greater ORs for mortality (1.65, 1.91, and 2.32, respectively) than the normonatremia group (all P values < 0.05). However, later sodium levels (24 and 72 h after CRRT) did not predict 30-day mortality. Furthermore, the changes in sodium over 24 or 72 h, including the appropriate correction of dysnatremia, did not show any relationships with mortality, irrespective of baseline sodium level. Sodium level at the start of CRRT was a strong predictor of mortality. However, changes in sodium level and the degree of sodium correction were not associated with the mortality risk in the patients with CRRT.

Kruppel-like factor 2 (KLF2) regulates endothelial cell metabolism; endothelial dysfunction is associated with hypertension and is a predictor of atherosclerosis development and cardiovascular events. Here, we investigated the role of KLF2 in hypertensive nephropathy by regulating KLF2 expression in human primary glomerular endothelial cells (hPGECs) and evaluating this expression in the kidney tissues of a 5/6 nephrectomy mouse model as well as patients with hypertension. Hypertension-mimicking devices and KLF2 siRNA were used to downregulate KLF2 expression, while the expression of KLF2 was upregulated by administering simvastatin. After 4 mmHg of pressure was applied on hPGECs for 48 h, KLF2 mRNA expression decreased, while alpha-smooth muscle actin (αSMA) mRNA expression increased. Apoptosis and fibrosis rates were increased under pressure, and these phenomena were aggravated following KLF2 knockdown, but were alleviated after simvastatin treatment; additionally, these changes were observed in angiotensin II, angiotensin type-1 receptor (AT1R) mRNA, and interleukin-18 (IL-18), but not in angiotensin type-2 receptor mRNA. Reduced expression of KLF2 in glomerular endothelial cells due to hypertension was found in both 5/6 nephrectomy mice and patients with hypertensive nephropathy. Thus, our study demonstrates that the pressure-induced apoptosis and fibrosis of glomerular endothelial cells result from angiotensin II, AT1R activation, and KLF2 inhibition, and are associated with IL-18.

Background: Terlipressin, as a prodrug of vasopressin, has agonistic effects on the V1 receptor and partial agonistic effects on renal vasopressin V2 receptors. However, its effects on serum sodium concentration are controversial. Methods: This study retrospectively investigated 127 patients with liver cirrhosis to examine the incidence and risk factors for the decrease in serum sodium level following terlipressin administration. Results: Terlipressin was prescribed for bleeding control (99) and management of hepatorenal syndrome (28). Serum sodium level decreased from 134.0 ± 6.5 mmol/L to 130.4 ± 6.2 mmol/L during or after terlipressin treatment (P < 0.001) in all patients. In 45 patients (35.4%), the serum sodium concentration decreased by > 5 mmol/L, in 29 patients (22.8%); by 5–10 mmol/L; and in 16 patients (12.6%), by > 10 mmol/L. Five patients in the latter group showed neurological manifestations. In the univariate analysis, several factors including age, purpose of use, serum creatinine, and Model for End-Stage Liver Disease score, representing liver function, were significantly associated with the decrease in serum sodium after terlipressin administration. However, a multivariate analysis revealed that only initial sodium level was the most powerful predictor of terlipressin-induced reduction in serum sodium. Conclusion: An acute reduction in serum sodium concentration was not uncommon during terlipressin treatment, and the baseline serum sodium level was closely related to the reduction in serum sodium concentration.