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Fanconi Syndrome
Published in Charles Theisler, Adjuvant Medical Care, 2023
Fanconi syndrome (FS), also called Fanconi’s renotubular syndrome, is a kidney disorder in which excess amounts of glucose, cysteine, galactose, fructose, bicarbonate, phosphates (phosphorus salts), uric acid, potassium, and certain amino acids are lost in the urine to be excreted. Normally, these substances are reabsorbed back into the bloodstream by the proximal tubules in the kidneys. A child with FS may experience slow growth, failure to thrive, and chronic kidney disease along with increased urine production, weakness, and bone abnormalities.1 There are hereditary and acquired forms of this disorder. In general, treatment involves maintaining fluid balance through replacement of the nutrients lost in the urine. In severe cases, some people may develop kidney failure and need a kidney transplant.1
Diabetic Nephropathy
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Overall, the prevalence of CKD is estimated to affect 14.8% of adults in the United States. African American, Native American, and Asian American people have higher incidence and prevalence of CKD than other groups. Global prevalence is estimated as being between 11% and 15% of the population, with most cases being stage 3 at diagnosis. Patients with end-stage kidney disease that require kidney transplants number between 4.9 and 7.1 million worldwide. Areas of the world with the highest amount of cases include Europe, the United States, Canada, Australia, Japan, South Korea, and the Oceanic countries. Most people that are affected are older than 40 years, since the kidneys naturally begin to lose filtration by about 1% per year after the age of 40, and conditions that damage them such as diabetes are also more common with aging. Though various studies have given different results, most studies show that chronic renal failure is slightly more common in women than in men.
Concepts and Issues in Adherence
Published in Lynn B. Myers, Kenny Midence, Adherence to Treatment in Medical Conditions, 2020
Rovelli et al. (1989) assessed adherence to immunosuppressive medications in organ transplant recipients in two studies: a retrospective review and a prospective study. In the retrospective review of 260 patients who had received kidney transplants, they assessed whether patients kept follow-up appointments and whether they had been adherent in taking immunosuppressant medication. Medication adherence was measured by self-report by patient, family report and doctor’s judgement. From our previous discussion, it may be assumed that using self-report and doctor’s judgement as measures would probably result in an overestimation of adherence. With this limitation in mind, the researchers found that 18% of patients were considered to be non-adherent to both follow-ups and medication. Three months post-transplant, 91% of these patients either rejected or died compared with 18% of adherent patients.
Fecal β-glucuronidase activity differs between hematopoietic cell and kidney transplantation and a possible mechanism for disparate dose requirements
Published in Gut Microbes, 2022
Mohammad Haneef Khan, Guillaume C. Onyeaghala, Armin Rashidi, Shernan G. Holtan, Alexander Khoruts, Ajay Israni, Pamala A. Jacobson, Christopher Staley
We compared β-glucuronidase activity from stool samples of patients receiving MMF and tacrolimus post-HCT or kidney transplant. We hypothesized that, based on observed differences in therapeutic dosing regimens between transplantation types, β-glucuronidase activity would differ between transplant types. We observed that fecal β-glucuronidase activity was over two-fold lower in HCT patients (3.50 ± 3.29 nmol/h/g) than in kidney transplant patients (8.48 ± 6.21 nmol/h/g, P = .001; Figure 1). Previous studies have found an association of distinct intestinal microbiota with clinical outcomes including infectious complications in HCT recipients19–21 and dosing of the IS drug tacrolimus (TAC) in kidney transplant recipients.22 In addition, greater abundances of the genera Blautia and Enterococcus, and decreasing abundances of clostridia have been associated with a lower incidence of GVHD-related mortality in HCT patients.19–21 In kidney transplant patients, Lee, et al.22 hypothesized that the abundance of Faecalibacterium prausnitzii was associated with a healthy and diverse colon and found a positive correlation between TAC dosage and F. prausnitzii. This hypothesis was tested in vitro by Guo, et al.23 with results suggesting involvement of F. prausnitzii in metabolism of TAC. Taken together, these results suggest that improved understanding of the role of the microbiota in biotransformation and transporting IS drugs will be critical to inform precision therapy to maximize efficacy.
Effects of perioperative dexmedetomidine infusion on renal function and microcirculation in kidney transplant recipients: a randomised controlled trial
Published in Annals of Medicine, 2022
Yin-Chin Wang, Ming-Jiuh Wang, Chih-Yuan Lee, Chien-Chia Chen, Ching-Tang Chiu, Anne Chao, Wing-Sum Chan, Meng-Kun Tsai, Yu-Chang Yeh
This prospective, randomised, controlled, single-blinded, open-label study was approved by the Research Ethics Committee of National Taiwan University Hospital, Taipei, Taiwan (Ethical Committee number 201512039MINB). This study was registered on the ClinicalTrials.gov protocol registration system (ID: NCT02707809). Patients undergoing kidney transplants were evaluated for eligibility. We excluded patients younger than 20 years or older than 70 years, and those with an allergy to dexmedetomidine, refractory bradycardia (heart rate below 60 beats per minute after treatment), and severe atrioventricular block (Mobitz type II and III). Written informed consent was obtained from all participants. The study was conducted and reported in accordance with the CONSORT recommendations [16]. The histidine-tryptophan-ketoglutarate solution was used for flushing and perfusion of the donor kidney, and the donor's kidney was kept in static cold storage before transplant surgery.
Uncover diagnostic immunity/hypoxia/ferroptosis/epithelial mesenchymal transformation-related CCR5, CD86, CD8A, ITGAM, and PTPRC in kidney transplantation patients with allograft rejection
Published in Renal Failure, 2022
Long He, Boqian Wang, Xueyi Wang, Yuewen Liu, Xing Song, Yijian Zhang, Xin Li, Hongwei Yang
In recent years, kidney transplantation has been considered as the best therapeutic intervention for patients with end-stage organ failure [1]. However, kidney transplantation brings the risk of allograft rejection. If leaving unchecked, allograft rejection reaction can destroy the graft. With the use of immunosuppressive agents, the incidence of transplant rejection has reduced [2]. Although the annual survival rate of kidney transplant has reached more than 90%, there is a 4–5% loss of function of the kidney graft. The 5-year survival rate of kidney transplant is 70%, whereas the 10-year survival rate is only 50% [2]. Regular monitoring of serum creatinine is an insensitive predictor and only increases upon the deficiency in kidney function [3]. Thus, it is important to identify potential diagnostic and therapeutic markers that associated with different molecular mechanisms in the process of allograft rejection in kidney transplant patients.