Chronic kidney disease (CKD) causes considerable morbidity, mortality, and health expenditures worldwide. Obesity is a significant risk factor for CKD development, partially explained by the high prevalence of diabetes mellitus and hypertension in obese patients. However, adipocytes also possess potent endocrine functions, secreting a myriad of cytokines and adipokines that contribute to insulin resistance and induce a chronic low-grade inflammatory state thereby damaging the kidney. CKD development itself is associated with various metabolic alterations that exacerbate adipose tissue dysfunction and insulin resistance. This adipose-renal axis is a major focus of current research, given the rising incidence of CKD and obesity. Cellular senescence is a biologic hallmark of aging, and age is another significant risk factor for obesity and CKD. An elevated senescent cell burden in adipose tissue predicts renal dysfunction in animal models, and senotherapies may alleviate these phenotypes. In this review, we discuss the direct mechanisms by which adipose tissue contributes to CKD development, emphasizing the potential clinical importance of such pathways in augmenting the care of CKD.

To address the ongoing shortage of organs available for replacement, xenotransplantation of hearts, corneas, skin, and kidneys has been attempted. However, a major obstacle facing xenotransplants is rejection due to a cycle of immune reactions to the graft. Both adaptive and innate immune systems contribute to this cycle, in which natural killer cells, macrophages, and T-cells play a significant role. While advancements in the field of genetic editing can circumvent some of these obstacles, biomarkers to identify and predict xenograft rejection remain to be standardized. Several T-cell markers, such as CD3, CD4, and CD8, are useful in both the diagnosis and prediction of xenograft rejection. Furthermore, an increase in the levels of various circulating DNA markers and microRNAs is also predictive of xenograft rejection. In this review, we summarize recent findings on the advancements in xenotransplantation, with a focus on pig-to-human, the role of immunity in xenograft rejection, and its biomarkers.

Purpose. Urinary tract infections (UTIs) are common in the first 6 months after renal transplantation, and there are only limited data about UTIs after transplantation in Saudi Arabia in general. Methods. A retrospective study from January 2017 to May 2020 with 6-month follow-up. Results. 279 renal transplant recipients were included. Mean age was 43.4±16.0 years, and114 (40.9) were women. Urinary stents were inserted routinely during transplantation and were removed 35.3±28 days postoperatively. Ninety-seven patients (35) developed urinary tract infections (UTIs) in the first six months after renal transplantation. Of those who developed the first episode of UTI, the recurrence rates were 57, 27, and 14 for having one, two, or three recurrences, respectively. Late urinary stent removals, defined as more than 21 days postoperatively, tended to have more UTIs (OR: 1.43, P: 0.259, CI: 0.762.66). Age >40, female gender, history of neurogenic bladder, and transplantation abroad were statistically significant factors associated with UTIs and recurrence. Diabetes, level of immunosuppression, deceased donor renal transplantation, pretransplant residual urine volume, or history of vesicoureteral reflux (VUR) was not associated with a higher incidence of UTIs. UTIs were asymptomatic in 60 but complicated with bacteremia in 6 of the cases. Multidrug resistant organisms (MDROs) were the causative organisms in 42 of cases, and in-hospital treatment was required in about 50 of cases. Norfloxacin+Bactrim DD (160/800mg) every other day was not associated with the lower risk of developing UTIs compared to the standard prophylaxis daily Bactrim SS (80/400mg). Conclusion. UTIs and recurrence are common in the first 6 months after renal transplantation. Age >40, female gender, neurogenic bladder, and transplantation abroad are associated with the increased risk of UTIs and recurrence. MDROs are common causative organisms, and hospitalization is frequently required. Dual prophylactic antibiotics did not seem to be advantageous over the standard daily Bactrim.

After renal transplantation, many patients experience adverse effects from maintenance immunosuppressive drugs. When these adverse effects occur, patient adherence with immunosuppression may be reduced and impact allograft survival. If these adverse effects could be prospectively monitored in an objective manner and possibly prevented, adherence to immunosuppressive regimens could be optimized and allograft survival improved. Prospective, standardized clinical approaches to assess immunosuppressive adverse effects by health care providers are limited. Therefore, we developed and evaluated the application, reliability and validity of a novel adverse effects scoring system in renal transplant recipients receiving calcineurin inhibitor (cyclosporine or tacrolimus) and mycophenolic acid based immunosuppressive therapy.

Purpose. To evaluate the impact of early (3 weeks) urinary stent removal on urinary tract infections (UTIs) post renal transplantation. Methods. A retrospective study was performed including all adult renal transplants who were transplanted between January 2017 and May 2020 with a minimum of 6-month follow-up at King Abdulaziz Medical City, Riyadh, Saudi Arabia. Results. A total of 279 kidney recipients included in the study were stratified into 114 in the early stent removal group (ESR) and 165 in the late stent removal group (LSR). Mean age was 43.4 ± 15.8; women: n: 114, 40.90%; and deceased donor transplant: n: 55, 19.70%. Mean stent removal time was 35.3 ± 28.0 days posttransplant (14.1 ± 4.6 days in the ESR versus 49.9 ± 28.1 days in LSR, ). Seventy-four UTIs were diagnosed while the stents were in vivo or up to two weeks after the stent removal “UTIs related to the stent” (n = 20, 17.5% in ESR versus n = 54, 32.7% in LSR; ). By six months after transplantation, there were 97 UTIs (n = 36, 31.6% UTIs in ESR versus n = 61, 37% in LSR; ). Compared with UTIs diagnosed after stent removal, UTIs diagnosed while the stent was still in vivo tended to be complicated (17.9% versus 4.9%, : 0.019), recurrent (66.1% versus 46.3%; : 0.063), associated with bacteremia (10.7% versus 0%; : 0.019), and requiring hospitalization (61% versus 24%, : 0.024). Early stent removal decreased the need for expedited stent removal due to UTI reasons (rate of UTIs before stent removal) (n = 11, 9% in the early group versus n = 45, 27% in the late group; ). The effect on the rate of multidrug-resistant organisms (MDRO) was less clear (33% versus 47%, : 0.205). Early stent removal was associated with a statistically significant reduction in the incidence of UTIs related to the stent (HR = 0.505, 95% CI: 0.302-0.844, ) without increasing the incidence of urological complications. Removing the stent before 21 days posttransplantation decreased UTIs related to stent (aOR: 0.403, CI: 0.218-0.744). Removing the stent before 14 days may even further decrease the risk of UTIs (aOR: 0.311, CI: 0.035- 2.726). Conclusion. Early ureteric stent removal defined as less than 21 days post renal transplantation reduced the incidence of UTIs related to stent without increasing the incidence of urological complications. UTIs occurring while the ureteric stent still in vivo were notably associated with bacteremia and hospitalization. A randomized trial will be required to further determine the best timing for stent removal.

Premalignant lesions of the gastrointestinal tract are a group of disorders which act as the harbinger of malignant tumors. They are the ground-zero of neoplastic transformation, and their identification and management offer patients the best opportunity of blocking the progress of cancer. However, diagnoses of some of these conditions are hard to make, and their clinical importance is difficult to assess. Recent reports indicated that several claudin proteins have altered expressions in many cancers, including esophageal, gastric, colon, liver, and pancreatic cancers. The early identification of the aberrant expression of these proteins could lead to the early diagnosis and management of gastrointestinal tumors. Specifically, claudins -1, -2, -3, -4, and -18 are frequently overexpressed in gastrointestinal preneoplastic lesions. These altered expressions have shown clinical value in several tumors, providing diagnostic and prognostic information. In this article, we review the literature on the aberrant expression of claudins in preneoplastic lesions of the gastrointestinal tract. Additionally, we summarize their diagnostic and prognostic implications.