Use of lung ultrasound to assess volume status and its association with physical examination in patients with chronic kidney disease.

Introduction: Defining the optimal hydration status in patients with chronic kidney disease (CKD) is challenging, and the quest for an objective accurate method continues. Lung ultrasound (LUS) is a well-validated technique to estimate volume status. Previous studies examining the relationship between LUS and physical examination demonstrated conflicting results. We aimed to evaluate the correlation between LUS results and physical examination for assessing volume status in patients with CKD, and to compare different LUS protocols. Methods: A prospective, single-center trial correlating physical examination findings to LUS results in different CKD groups, including non-dialysis and dialysis patients. Hemodialysis patients were tested twice, before and after dialysis, to compare results with ultrafiltration volume. Different LUS protocols were performed and compared, including 16-, 12-, and 8-zone measurements. Results: We recruited 175 participants. A strong positive correlation was demonstrated between 16- and 12-zone protocols [r = .91 (P < .001)] and between 12- and 8-zone protocols (r = .951, P < .001). Correlation was significant in various CKD groups. While blood pressure did not correlate with LUS score, there was a significant correlation between LUS and other components of the physical examination including lung crackles (OR = 1.15 (95%CI 1.096-1.22), P < .01), pleural effusion (OR = 1.15 (95%CI 1.09-2.13), P < .01) and peripheral edema (r = .24, P < .001). Ultrafiltration volume did not correlate significantly with change in LUS scores pre- and post-dialysis (r = .169, P = .065). Conclusion: Most components of physical examination findings correlated with extravascular lung water assessment on LUS in CKD patients. The use of a simplified pragmatic LUS protocol may facilitate LUS use in clinical practice.

The Long-Term Outcome of Kidney Transplant Recipients in the Eighth Decade Compared With Recipients in the Seventh Decade of Life.

BACKGROUND: With the aging of the population, more older patients are being considered for kidney transplantation; therefore, it is crucial to evaluate the risks and benefits of transplantation in this population. This study aimed to assess long-term outcomes of kidney transplantation in a cohort of patients who underwent kidney transplantation at age >70 years, compared with patients aged 60 to 69 years at transplantation. METHODS: Included in the study were 261 consecutive kidney transplant recipients: 52 were aged >70 years, and 209 were aged 60 to 69 years at transplantation. Data were collected retrospectively and analyzed using multivariate logistic regression to identify potential outcome risk factors. RESULTS: The number of transplants in both groups increased during the study period. Mortality after transplantation was strongly correlated to age (hazard ratio [HR] = 1.11; 95% CI, 1.05-1.18; P < .001), deceased donor (HR = 2.0; 95% CI, 1.1-3.8; P = .034), and pretransplant diabetes (HR = 2.9; 95% CI, 1.7-4.9; P = .001). Recipients aged >70 years had an increased risk of death censored graft failure (HR = 2.98; 95% CI, 1.56-5.74; P = .001). In living donor transplants, 3-year survival was 80% in recipients age >70 years, compared with 98% in the 60- to 69-year group. Five-year survival was 71% and 92%, respectively. In deceased donor transplants, 3-year survival was 63% and 78%, and 5-year survival was 58% and 72%, respectively. The risk of malignancy (excluding nonmelanotic skin cancer) was nearly triple in the age >70 years group (HR = 2.96; 95% CI, 1.3-6.8; P = .01). CONCLUSIONS: Patient and graft survival in kidney recipients in the eighth decade is worse compared with recipients in the seventh decade of life. However, it is improved with living kidney donation.

Renal Tubular CD24 Upregulation Aggravates Folic Acid Induced Acute Kidney Injury: A Possible Role for T Regulatory Cells Inhibition in Mice.

Acute kidney injury (AKI) is characterized by cell death and inflammation. CD24 is a protein induced during tissue damage and is not expressed in mature renal tissue. We explored the role of CD24 in the pathogenesis of folic acid-induced AKI (FA-AKI) in mice. A single Intraperitoneal (IP) injection of folic acid induced AKI in WT and CD24-/- mice. Renal function tests, histological analysis, immunohistochemistry, Western blot analysis, and ELISA were performed to assess the severity of renal damage and the intensity of the inflammatory response. FA-AKI induced CD24 in the distal tubular epithelial cells. Compared to WT mice, FA-AKI CD24-/- mice exhibited an attenuated reduction in renal function and histological injury, lower serum IL-10 and interferon γ, and decreased expression of renal TNFα. In contrast, renal and systemic IL-33 upregulation were augmented. CD24-/- FA-AKI animals exhibited increased splenic margination and renal infiltration of regulatory T cells (Tregs). At day 7, FA-AKI CD24-/- mice exhibited increased expression of tubular pro-apoptotic and decreased anti-apoptotic proteins compared to WT animals. Anti-CD24 antibody administration to FA-AKI mice attenuated the decrease in renal function as well as the histological injury. Renal biopsies from patients with ATN stained strongly for CD24 in the distal tubules. In conclusion, during AKI, upregulation of CD24 promotes renal inflammation through inhibition of Treg infiltration and diversion of cell death towards necrosis rather than apoptosis. Neutralization of CD24 may prove a target for future therapies in AKI.