Growth failure is a marked feature in children with CKD. Kidney transplantation (KTx) is the therapeutic option that provides the greatest benefits to the pediatric population. Considering the importance of this subject, a systematic search of the literature was carried out on the principal databases from January 2015 to December 2020. The following descriptors in health science (DECs) from the VHL portal (library virtual health) were applied: pediatric kidney transplantation (PKTx), growth and development. It was found that among the etiologies, congenital abnormalities of the kidneys and urinary tract (CAKUT) were the main causes of loss of renal function. The highest mean age was 15.52 ± 1.8 years. The type of donor was reported in only 3 studies, in 1 of which the living donor was predominant. The immunosuppression (ISS) schemes after PKTx were similar in the studies, the triple scheme with corticoid, calcineurin inhibitor and anti-proliferative being used in most of them. The use of GH did not occur in 4 of the 9 studies. We could conclude that weight and height gain after PKTx is an important outcome to be evaluated. In underdeveloped or developing countries where, in addition to chronic disease, we find nutritional and economic precariousness, it is very important to know the factors that greatly contribute to the impairment of height and weight gain of these patients. Controlled and randomized studies that find answers for the control of pediatric patients after PKTx and that can be applied in our country are desired.

Background: A diuretic strategy is needed that is superior to current clinical care in the management of cardiorenal syndrome. Current HF guidelines do not provide any standard protocol for diuretic dosing. Aim: To determine if a protocolized diuretic treatment strategy (ProDiuS), compared to usual care (UC), results in improved decongestion, clinical outcomes, and health-related quality of life (HRQOL), while preserving renal function in hospitalized patients with cardiorenal syndrome. Materials and Methods: This trial was a prospective randomized single-blind trial of participants hospitalized for cardiorenal syndrome from November 1, 2013 to July 9, 2015. Participants were randomized to ProDiuS vs. UC and followed daily in hospital, and at 1-month and 3-month follow-up. ProDiuS was a stepped diuretic strategy targeting daily urine output of 3-5 L/day. UC was care at the discretion of treating providers. The primary outcome, change in body weight (kg) from randomization to 96 hours (day 4), was compared between the ProDiuS and UC groups using the t-test. Data analysis for secondary outcomes between the two groups were conducted using the t-test or Wilcoxon rank sum test depending on whether data was skewed for continuous variables, as well as linear regression modeling. For ordinal variables or proportions, data were analyzed using the exact chi-square test and logistic regression modeling. For mortality, time to death was analyzed as time-to-event data, with censoring at the time of death, date of last follow-up, or the end of the study (3 month follow-up), using Kaplan-Meier curves and log-rank tests, and Cox proportional hazards models to adjust for continuous and discrete covariates in the survival analysis. Results: The study did not enroll the prespecified number of subjects due to slow recruitment. Out of 786 prescreened patients, 19 participants were included in the trial. There were no significant differences in baseline characteristics. Mean age was 68.7±7.3 years and 72.2% were male. There was borderline higher change in body weight from baseline to day 4 or discharge in ProDiuS vs. UC (-6.12 vs. -2.07 kg; p=0.05). Net negative fluid balance, length of hospitalization, HF rehospitalizations, mortality, acute kidney injury, adverse outcomes, and HRQOL scores were similar between groups. Conclusion: Due to small sample size, firm conclusions cannot be drawn. However, these findings suggest that ProDiuS results in similar clinical and HRQOL outcomes as UC in HF patients treated at a large tertiary medical center in the short term. This trial was conducted in an advanced HF population on specialized HF services, which may have attenuated the efficacy of ProDiuS vs. UC. Further studies with larger sample size and more diverse HF populations are needed to determine the efficacy and safety of ProDiuS. Several lessons learned in attempting to design a trial of protocolized diuretic strategy in the cardiorenal population are discussed.

The inspiration to write this article came after I took my Chinese herbal medicine course, which I finished in early 2002, where I was able to fully understand the issues of the energy aspect of our organs. According to the most renowned physicists, such as Albert Einstein (1879-1955), he says that everything that exists in our universe is composed of energy, including the human being. If we think like Hippocrates (c. 460 bce - c. 375 bce), the father of medicine, he says that “we should consider the oldest medicines before the practice of current medicine”. For this reason, I will write this article using the teachings of traditional Chinese medicine, which has existed for more than five thousand years, to write the other energy functions of the Kidney, which Western medicine still does not study, because according to Western medicine reasoning, the Kidney has the function of filtering the blood and throwing out through the urine, all the components of the blood that are in excess in the body, to maintain the homeostatic integrity.

β2m is a precursor protein of the dialysis-related amyloidosis (DRA) and β2m lacking the N-terminal six residues of the mature protein (ΔN6β2m) is a one of amyloidogenic variant of β2m. In the previous study, we had showed an unfolding in the C-terminal of ΔN6β2m using the specific monoclonal antibody for ΔN6β2m. We had also reported firstly an aptamer specific for ΔN6β2m. ΔN6β2m-aptamers specifically and tightly bound to ΔN6β2m and inhibited fibril formation. These results suggest the potential of ΔN6β2m-aptamers as reagents for therapeutic tools to prevent amyloid deposits in dialysis patients.

The mineral and bone disease of chronic kidney disease (CKD-MBD) is a combination of three components: abnormalities in calcium, phosphorus, PTH, fibroblast growth factor 23 (FGF23) and vitamin D metabolism; abnormalities of bone metabolism, mineralization, volume, growth and strength; and vascular and other soft tissue calcification. During the natural course of kidney disease, there is an increase in FGF23 levels, inhibition of calcitriol production, secondary hyperparathyroidism, hypocalcemia and hyperphosphatemia. These changes have consequences on the cardiovascular and bone systems. Regarding cardiovascular disease, left ventricular hypertrophy is highlighted, associated with an increase in FGF23 and vascular calcification, directly related to hyperphosphatemia. The main types of bone disease are cystic fibrous osteitis (high turnover) and adynamic bone disease (low turnover), both of which are associated with a high risk of fracture in this population. Successful kidney transplantation (KT) does not fully correct the mineral, bone and cardiovascular abnormalities generated by CKD-MBD. In the first months after transplantation, PTH and FGF23 levels remain elevated in most patients. There is an increase in the production of calcitriol by the graft. These are the main alterations responsible for a mineral phenotype that resembles primary hyperparathyroidism, with hypercalcemia, hypophosphatemia and elevated PTH levels. Cardiovascular disease does not revert after KT and the transplant patient has a higher cardiovascular risk than the general population. In relation to bone disease, in addition to the pre-existing bone alteration, specific factors of the post-KT period add damage to the bone, especially the use of corticosteroids. The main types of bone disease in renal transplant patients are bone fracture, renal osteodystrophy, osteoporosis and osteonecrosis. CKD-MBD is a complex disease that affects patients with CKD, increasing their morbidity and mortality. KT does not fully reverse the disease and still adds other specific risk factors that make its approach challenging. This review sought to show the association between the bone mineral disease of chronic kidney disease and the risk of fractures, vascular and other tissue calcifications, graft dysfunction and kidney transplant patient mortality.

Anemia is a common complication in chronic kidney disease (CKD) and has been associated with a reduced quality of life [1] as well as worse survival [2] and increased morbidity and mortality [3]. The prevalence of anemia is more severe as the estimated glomerular filtration rate (eGFR) declines and is 8.4% at stage 1 to 53.4% at stage 5. Similar data is observed in a more recent paper by the CKD Prognosis Consortium which also observed an increased prevalence of anemia among diabetic patients, independent of eGFR and albuminuria [4]. In CKD patients, EPO deficiency starts early in the course of CKD and appears initially, when eGFR falls below 30ml/min/1.73m2, this deficiency becomes more severe [5]. This absolute EPO deficiency can be caused by a decrease EPO production and /or errors in EPO sensing. CKD produces an alteration in oxygen delivery to the kidneys and results in adaptation of renal tissue to consume less oxygen and subsequent maintenance of normal tissue oxygen gradient. As a consequence, prolyl-hydroxylase domain (PHD) enzymes which regulates HIF activity remain active, the HIF heterodimer is not formed and the EPO gene is not activated [6]. Some CKD patients may also present with a functional EPO deficiency or EPO resistance, where normal range. EPO levels co-exist with low hemoglobin levels indicating a blunted bone marrow response to endogenous and exogenous EPO. Mechanisms hypothesized for EPO resistance include presence of pro-inflammatory cytokines thought to induce apoptosis and down regulation of expression of EPO receptor.

Physicians often face ethical dilemmas when providing advice regarding withdrawal of care. In the nephrology world, we are especially at risk due to the high mortality of our patients. Yet our training tends to lag behind in certain aspects of end of life goals of care discussions. Some of our patients enquire regarding physician-assisted death (PAD) as an option and our current training does not enable us to provide an informed answer. In end-stage-renal patients, opting out of dialysis will certainly result in a rapid demise for most, however, some patients request further assistance. We updated information to be, at the least, able to help our most vulnerable patients with the information. The process of dying, sometimes prolonged to weeks, is a very painful procedure, and not under the patient's control. Withdrawal of care, even with the best palliative care options, does not always result in the control that physician-assisted death (PAD) can provide. It appears as a reasonable option to some patients at the end of life. Is PAD a part of doing “everything that can be done” to keep a patient comfortable (as a part of comfort goals of care)? The provision exists in certain states. However, moving to another state at the end of life is not really practical or even a kind option to consider. A physician can have moral and ethical dilemma around these queries. Our paper discusses available data on this issue intending to empower providers with optimal information. Professional position guidelines do not agree with or recommend physician-assisted-death. This knowledge helps clear the conscience of providers knowing that, at the least, we are doing what most other physicians would do. The question remains: Is PAD a part of “everything that can be done” for the patient? This manuscript aims to update regarding this issue especially as there have been recently active discussions worldwide with the launch of newer technology-assisted death. We present a case modified extensively from real life cases for academic discussion only. We do not provide any recommendation regarding the practice.

The aim of this narrative review is to shed light on the correlation between metabolic-associated fatty liver disease (MAFLD) and chronic kidney disease progression (CKD). There is robust evidence from the current and recent literature that MAFLD is strongly associated with CKD incidence and progression regardless of other confounding factors such as DM, hypertension, dyslipidemia, age, and gender. we believe that MAFLD and CKD are two important health issues, both have a global and economic burden that will continue to rise over the coming years. Primary and secondary care physicians, particularly nephrologists should be fully aware of the impact of MAFLD on CKD patients so they can participate actively in the management plan of these patients to reduce the comorbidities and economic costs associated with it. Methodology: The review identified and included the most recent few studies that described the problem of interest. Recommendations are given based on our perception, interpretation, and synthesis of data from the reviewed literature. Results: The existence of a strong correlation between MAFLD and CKD was persistent across all the reviewed studies and articles. This correlation was independent of other traditional risk factors such as hypertension, diabetes mellitus, hyperlipidemia, gender, and age. Conclusion: The global prevalence of MAFLD among the general population is high reaching 30% and almost 50% of CKD patients have MAFLD. There is a strong and independent association between MAFLD and CKD incidence and progression, thus patients diagnosed with CKD should be screened for MAFLD and managed accordingly to prevent and delay CKD progression.

Background: Hypertensive nephrosclerosis is chronic impact of high blood pressure on the kidney. The objective of this study was to determine prevalence, clinical presentation, and evolution of hypertensive nephrosclerosis in patients admitting in our service. Patients and Methods: We performed a retrospective, descriptive and analytical study in nephrology department of Aristide Le Dantec University Hospital in Dakar during a period of 05 years. Patients with long-term hypertension, hypertensive retinopathy, left ventricular hypertrophy, and progressive kidney failure were included. Results: 461 patients were included. Hospital prevalence was 7.7%. Mean age was 56.95±13.23 years and sex ratio was 1.07. Uncontrolled high blood pressure has been found in 400 patients. Mean systolic blood pressure was 168.34 ± 27.57 mmHg. Mean diastolic blood pressure was 97.28±19.59 mmHg. On the urine dipstick, 44 patients had proteinuria (<2cross). Mean GFR, was 22.02±17.78 ml/min. Antihypertensive treatment was administered as bitherapy in 232 patients (50.3%). On admission, 47 patients (10.2%) had already started dialysis. At 12 months, 406 patients were regularly followed. Blood pressure was normal in 138 patients and serum creatinine decreased in 74 patients. Advanced age (p=0.0001) and female gender (p =0.0001) were correlated with a low level of GFR. The high 24 hours proteinuria level was unfavorable factor on GFR (p = 0.004). Conclusion: This study shows a high prevalence of hypertensive nephropathy in our study population. His evolution to end stage of kidney disease is inevitable, hence the importance of prevention and early management of hypertension in black subjects

Tumor size, histologic grade, and TNM classification characterize kidney tumors and provide a useful prognosis for predicting survival in research and medicine. Our objective was to determine the postoperative survival of operated patients with a diagnosis of clear cell renal carcinomas (CCRC) and to evaluate its relationship with other prognostic factors. Age, sex, clinical presentation, size, Fuhrman nuclear grade, tumor-nodule-metastasis (TNM) stage, and the presence of local invasion were retrospectively analyzed in 66 patients operated on for clear cell renal carcinomas. Clinical follow-up was performed for 5 years to determine postoperative survival. During the follow-up period, 17 deaths occurred, with the cancer-specific survival rate being 77%. The presenting symptoms of the tumor that led to the diagnosis were not related to postoperative survival. The estimated survival for stages T2 was 100%, for T1 it was 93%, and for T3 it was 55%. No patients were found in stage T4. The lower Fuhrman grades (I and II) had an 85% survival rate, while the higher grades (III and IV) had a 53% survival rate. Survival rates also varied depending on the type of adjacent tissue that was affected. Specifically, survival decreased to 80% when infiltrating the renal capsule, 70% when infiltrating the perirenal tissues, and 28% when invading the renal vein. We can conclude that tumor size in CRCC is not a prognostic factor that allows determining postoperative survival independently, and for this reason, it should be considered as a variable that acquires importance when evaluated together with the presence of vascular invasion or adjacent tissues. We can confirm that the Fuhrman Histological Grade is useful as an independent parameter of survival when grouped into low and high grades.