Uremic Patients Research Articles

Uremic and Post-Transplant Gastropathy in Patients With Chronic Kidney Disease and End-Stage Renal Disease.

Gastrointestinal (GI) mucosal lesions are common in chronic kidney disease (CKD), end-stage renal disease (ESRD), and in post-renal transplant period. However, etiology of mucosal lesions pre- and post-transplant is very different. Gastropathy in non-transplant ESRD patients usually develops because of uremia, chronic anemia, and fluctuations in the gastric blood supply during hemodialysis, eventually leading to uremic gastritis. Gastropathy in post-transplant patients tends to be associated with immunosuppressive therapies.Helicobacter pylori infection is more prevalent in uremic patients than in post-transplant patients. Uremia can also lead to uremic arteriolopathy and autonomic nervous system dysfunction, which can present with GI symptoms mimicking uremic gastropathy. Post-transplantation immunosuppressive therapies have been linked to GI mucosal lesions as well. These lesions carry a poor prognostic factor disrupting the function of the GI tract, which in turn affects the pharmacokinetics of the immunosuppressive drugs eventually leading to poor graft survival and increased mortality. Mycophenolate mofetil is one of the agents more associated with intestinal erosions.Recognizing uremic gastropathy and intervening early helps prevent post-transplant GI complications. Acid controlling therapies can be an effective prophylaxis against both gastropathies. Using enteric-coated formulation for immunosuppressive agents may slow down the mucosal insult. Treatment of H. pylori in both patient populations may help prevent further mucosal injury. Lastly, timely screening for symptoms may help start treatment early and prevent progression to serious gastropathy.

TREATING HYPERPROLACTINEMIA DOESN’T IMPROVE SEXUAL FUNCTION IN END STAGE RENAL DISEASE PATIENTS

Chronic kidney disease is associated with gonadal dysfunction. Patient usually present with deceased libido, erectile dysfunction & defective ejaculation. Significant derangements of the hypothalamic pituitary axes is commonly identified in uremic patients with reduced total & free serum testosterone levels and increased LH & FSH levels. Elevated levels of prolactin is usually seen in ESRD & is thought to contribute to the high prevalence of hypogonadism & sexual dysfunction. This study aims to evaluate the effect of treatment of hyperprolactinemia on sexual function in ESRD patients.

A combined microRNA and target protein-based panel for predicting the probability and severity of uraemic vascular calcification: a translational study.

Vascular calcification (VC) increases the future risk of cardiovascular events in uraemic patients, but effective therapies are still unavailable. Accurate identification of those at risk of developing VC using pathogenesis-based biomarkers is of particular interest and may facilitate individualized risk stratification. We aimed to uncover microRNA (miRNA)-target protein-based biomarker panels for evaluating uraemic VC probability and severity. We created a three-tiered in vitro VC model and an in vivo uraemic rat model receiving high phosphate diet to mimic uraemic VC. RNAs from the three-tiered in vitro and in vivo uraemic VC models underwent miRNA and mRNA microarray, with results screened for differentially expressed miRNAs and their target genes as biomarkers. Findings were validated in original models and additionally in an ex vivo VC model and human cells, followed by functional assays of identified miRNAs and target proteins, and tests of sera from end-stage renal disease (ESRD) and non-dialysis-dependent chronic kidney disease (CKD) patients without and with VC. Totally 122 down-regulated and 119 up-regulated miRNAs during calcification progression were identified initially; further list narrowing based on miRNA-mRNA pairing, anti-correlation, and functional enrichment left 16 and 14 differentially expressed miRNAs and mRNAs. Levels of four miRNAs (miR-10b-5p, miR-195, miR-125b-2-3p, and miR-378a-3p) were shown to decrease throughout all models tested, while one mRNA (SULF1, a potential target of miR-378a-3p) exhibited the opposite trend concurrently. Among 96 ESRD (70.8% with VC) and 59 CKD patients (61% with VC), serum miR-125b2-3p and miR-378a-3p decreased with greater VC severity, while serum SULF1 levels increased. Adding serum miR-125b-2-3p, miR-378a-3p, and SULF1 into regression models for VC substantially improved performance compared to using clinical variables alone. Using a translational approach, we discovered a novel panel of biomarkers for gauging the probability/severity of uraemic VC based on miRNAs/target proteins, which improved the diagnostic accuracy.

Restless Leg Syndrome in the Setting of Patients With End-Stage Renal Disease on Hemodialysis: A Literature Review.

Restless Leg Syndrome (RLS), or Willis-Ekbom disease (WED), is an irresistible urge to move the legs, predominantly while resting, sitting, or sleeping, which disrupts sleep and impairs quality of life. RLS can occur secondary to uremia in chronic kidney disease (CKD) patients due to inadequate hemodialysis. Early diagnosis is essential to prevent muscular atrophy and to improve the quality of life of RLS patients, especially those with end-stage renal disease (ESRD). Cardiac mortality high in uremic RLS patients due to associated discomfort and lowering the duration of hemodialysis treatment. This review focuses on and discusses the diagnosis, treatment, and associated comorbid conditions of uremic RLS. Though the exact pathophysiology is unknown, altered transferrin expression in the choroid plexus, increased glutamate levels in the thalamus, decreased opioid receptors, dopamine system dysfunction, calcium/phosphate imbalance, and single nucleotide polymorphisms in the BTBD9 and MEIS1 genes are a few nonconfirmatory pathophysiological concepts for uremic RLS. Nonpharmacological options include lowering the temperature of dialysate by 1 degree C and home-based therapies like massages, warm/cold baths, and aerobic exercises. Pharmacological therapy like dopamine agonists ropinirole and pramipexole reduces the symptoms effectively. However, surgical options like parathyroidectomy and renal transplantation are stated as the best treatment options in patients suffering from uremic RLS.

Differences between exhausted CD8+ T cells in hepatocellular carcinoma patients with and without uremia.

The purpose of this study was to explore the differences between exhausted CD8+ Tcells in hepatocellular carcinoma (HCC) patients with and without uremia. We enrolled 45 uremic patients who were recently diagnosed with HCC into the HCC+ uremia cohort and similar patients with HCC but without uremia into the HCC-only cohort. Lymphocytes were obtained from the two cohorts, and exhausted CD8+ Tcells, comprising PD-1+CD8+, TIM-3+CD8+, and LAG-3+CD8+ Tcells, were sorted and expanded invitro. After expansion, the proportions of PD-1+CD8+, TIM-3+CD8+, and LAG-3+CD8+ Tcells were significantly higher in the HCC-only cohort than in the HCC+ uremia cohort. CD8+ Tcells expressing PD-1, TIM-3, or LAG-3 showed increased tumor reactivity and release of interferon-γ invitro; however, these cells demonstrated weaker anti-tumor activity in HCC+ uremia patients than in HCC-only patients. Among the expanded lymphocytes, only the decreased proportion of PD-1+CD8+ Tcells significantly correlated with the HCC+ uremia cohort (odds ratio of 2.731, p= 0.009). We concluded that peripheral CD8+ Tcells expressing PD-1, TIM-3, or LAG-3 from the HCC+ uremia cohort were dysfunctional invitro. Among these populations, PD-1+CD8+ Tcells were most evident in HCC patients with uremia.

Intestinal dialysis in a uremic patient with diabetic nephropathy: A challenging case and a unique experience

Background: The beneficial use of intestinal (dietary) dialysis in patients with chronic renal failure has been increasingly described during the previous two decades. The cornerstone of the dietary management during intestinal dialysis is protein restriction that is compensated by adequate caloric intake. On the other hand the dietary management of diabetic patients includes calorie restriction that is compensated by adequate intake of proteins. Therefore, the dietary prescription of intestinal dialysis in diabetic patients can be challenging and are not expected to be convenient for many patients. However, a beneficial effect of intestinal in a patient with insulin dependent diabetes mellitus and symptomatic uremia has been reported. The aim of this paper is report a beneficial effect of intestinal dialysis in a diabetic uremic patient who had insulin dependent diabetes mellitus. Patients and methods: A 28-year-old female patient with insulin dependent diabetes mellitus, and symptomatic uremia and refused treatment with dialysis. She had marked weakness and was unable to stand and walk unaided. However, she didn’t have a life threatening uremic complication such as gastrointestinal bleeding or encephalopathy on referral. The patient was treated with intestinal dialysis. Results: The patient experienced amelioration of symptoms of uremia with improved general wellbeing in association with lowering of urea levels and creatinine during the period of therapy. She was unable to stand and walk unaided before the start of therapy, but she was able to climb more than 10 steps upstairs unaided after three weeks of therapy.

Intestinal dialysis in a uremic patient with diabetic nephropathy: A challenging case and a unique experience

Intestinal dialysis in a uremic patient with diabetic nephropathy: A challenging case and a unique experience

THU390 - Epidemiological evolution of viral hepatitis in uremic patients in Taiwan - the Formosa like group

THU390 - Epidemiological evolution of viral hepatitis in uremic patients in Taiwan - the Formosa like group

Proteomic Research in Peritoneal Dialysis.

Peritoneal dialysis (PD) is an established home care, cost-effective renal replacement therapy (RRT), which offers several advantages over the most used dialysis modality, hemodialysis. Despite its potential benefits, however, PD is an under-prescribed method of treating uremic patients. Infectious complications (primarily peritonitis) and bio-incompatibility of PD solutions are the main contributors to PD drop-out, due to their potential for altering the functional and anatomical integrity of the peritoneal membrane. To improve the clinical outcome of PD, there is a need for biomarkers to identify patients at risk of PD-related complications and to guide personalized interventions. Several recent studies have shown that proteomic investigation may be a powerful tool in the prediction, early diagnosis, prognostic assessment, and therapeutic monitoring of patients on PD. Indeed, analysis of the proteome present in PD effluent has uncovered several proteins involved in inflammation and pro-fibrotic insult, in encapsulating peritoneal sclerosis, or even in detecting early changes before any measurable modifications occur in the traditional clinical parameters used to evaluate PD efficacy. We here review the proteomic studies conducted thus far, addressing the potential use of such omics methodology in identifying potential new biomarkers of the peritoneal membrane welfare in relation to dialytic prescription and adequacy.

Burden in primary family caregivers caring for uremic patients on maintenance peritoneal dialysis.

Managing the burden of care for patients with chronic debilitating diseases is an important issue. Herein, we assessed the burden in primary family members caring for uremic patients on maintenance peritoneal dialysis. One hundred seventy caregivers and 170 patients were recruited. Self-perceived scoring along the Zarit Caregiver Burden Scale (ZCBS), World Health Organization Five-item Well-Being Index (WHO-5), and Warwick-Edinburgh Mental Well-being Scale (WEMWBS) were determined for caregivers. There was an inverse relationship between ZCBS and WHO-5 or WEMWBS scores in caregivers, suggesting that the higher the burden, the lesser the self-perceived well-being. One hundred two of 170 caregivers (60%) reported mild to moderate burden, indicating a common presence of mild to moderate caring-related mental and physical stress. Moreover, 31 caregivers (18.2%) reported moderate to severe burden. Several patient disease factors, including diabetes and frailty, increased caregiver burden, while insurance coverage and out-of-pocket medical costs were also positively correlated. Caregivers who lived with patients and spent longer hours in caring-related activities had higher burden scores, while regular exercise seemed to partially alleviate the burden. Our study clearly showed that caring for patients with maintenance peritoneal dialysis caused physical, mental, and social burden in family caregivers, with the extent of the stress being influenced by patients' disease severity and other demographic factors in both patients and caregivers.

Development of pancytopenia after single low-dose methotrexate therapy in patients with chronic kidney disease: a review of the literature

Methotrexate (MTX) is widely used in the treatment of both rheumatoid arthritis (RA) and psoriatic arthritis (PA) with a side effect of pancytopenia. However, very few cases of severe pancytopenia caused by low-dose MTX therapy have been described in chronic kidney disease. Pancytopenia occurred after using a single dose of MTX in three patients with chronic kidney dysfunction. While one patient died due to sepsis and multiple organ failure, the others recovered. The severity of MTX-inducedpancytopenia in our cases was likely related to the underlyingkidney disease. These cases suggest that uremic patients may develop severe fatal bone marrow toxicity even with a single dose of MTX. Therefore, close blood count monitoring after MTX treatment in this population would be beneficial.

Changes of miR‑155 expression in serum of uremic patients before and after treatment and risk factors analysis

The aim of the present study was to investigate the changes of miR-155 expression in the serum of uremic patients before and after treatment and analyze the risk factors of efficacy. A total of 116 uremic patients admitted to the People's Hospital of Chengyang (Qingdao, China) were enrolled in the study as the uremia group, and were treated by hemodialysis combined with hemoperfusion, and 127 healthy subjects who underwent health examination during the same period were selected as the normal group. Reverse transcription quantitative PCR was used to detect the serum miR-155 levels of all the subjects in the two groups before treatment and those of uremia patients after treatment. The changes of clinically related indicators and inflammatory factors in uremic patients before and after treatment and their correlation with miR-155 were investigated. The risk factors affecting the efficacy of treatment were analyzed. Serum miR-155 levels in the uremia group were higher than those in the normal group (P<0.001); the miR-155 level in patients after treatment was significantly lower than that before treatment (P<0.001), and it was positively correlated with efficacy (r=0.6873, P<0.05). The serum miR-155 level in the invalid group was higher than that in the effective group, and the sensitivity and specificity of miR-155 for predicting the efficacy before treatment were 64.71 and 87.88%, respectively. After treatment, the sensitivity and specificity of miR-155 for evaluating the efficacy were 76.47 and 88.89%, respectively. Clinically related indicators and inflammatory factor levels in uremic patients decreased significantly after treatment, and the expression levels before and after treatment were significantly correlated with miR-155. Clinically related indicators, inflammatory factors and miR-155 were all risk factors affecting efficacy. The expression level of miR-155 in serum was significantly upregulated. Findings of this study suggest that monitoring miR-155 may reflect the efficacy and inflammatory state effectively.

Human CD16+ monocytes promote a pro-atherosclerotic endothelial cell phenotype via CX3CR1-CX3CL1 interaction.

Monocytes are central for atherosclerotic vascular inflammation. The human non-classical, patrolling subtype, which expresses high levels of CD16 and fractalkine receptor CX3CR1, strongly associates with cardiovascular events. This is most marked in renal failure, a condition with excess atherosclerosis morbidity. The underlying mechanism is not understood. This study investigated how human CD16+ monocytes modulate endothelial cell function. In patients with kidney failure, CD16+ monocyte counts were elevated and dynamically decreased within a year after transplantation, chiefly due to a drop in CD14+CD16+ cells. The CX3CR1 ligand CX3CL1 was similarly elevated in the circulation of humans and mice with renal impairment. CX3CL1 up-regulation was also observed close to macrophage rich human coronary artery plaques. To investigate a mechanistic basis of this association, CD16+CX3CR1HIGH monocytes were co-incubated with primary human endothelium in vitro. Compared to classical CD14+ monocytes or transwell cocultures, CD16+ monocytes enhanced endothelial STAT1 and NF-κB p65 phosphorylation, up-regulated expression of CX3CL1 and interleukin-1β, numerous CCL and CXCL chemokines and molecules promoting leucocyte patrolling and adhesion such as ICAM1 and VCAM1. Genes required for vasodilatation including endothelial nitric oxide synthase decreased while endothelial collagen production increased. Uraemic patients' monocytes enhanced endothelial CX3CL1 even more markedly. Their receptor CX3CR1 was required for enhanced aortic endothelial stiffness in murine atherosclerosis with renal impairment. CX3CR1 dose-dependently modulated monocyte-contact-dependent gene expression in human endothelium. By demonstrating endothelial proatherosclerotic gene regulation in direct contact with CD16+ monocytes, in part via cellular CX3CR1-CX3CL1 interaction, our data delineate a mechanism how this celltype can increase cardiovascular risk.

In Vitro Detoxification Studies of p-Cresol by Intestinal Bacteria Isolated from Human Feces.

p-Cresol is a neurotoxic and nephrotoxic carcinogenic aromatic substance produced as a result of microbial fermentation in the intestine. The derivatives of p-cresol (p-cresyl sulphate or p-cresyl glucuronide) have a deleterious effect on renal failure patients undergoing hemodialysis. Human gut seems to be inhabited with a diverse microbial population capable of detoxifying many aromatic compounds. However, the knowledge on the role of gut microbes in metabolizing p-cresol is limited. Hence, the present study aims to investigate p-cresol detoxification by intestinal bacteria isolated from human feces. Three potential p-cresol tolerant isolates were selected and identified as Enterococcus faecalis strains (UTD-1, UTD-2 and UTD-3) by 16SrRNA gene sequencing. All three E. faecalis isolates decreased the p-cresol concentration (30µg/ml) at a higher rate with extracellular extracts (2.58-9.53µg/ml) as compared to intracellular (0.55-5.28µg/ml) extract. These three potential isolates also exhibited tolerance to gastrointestinal conditions for up to 60min. Added to its potential, the expression of virulent genes (esp, gelE, and cyl) was found to be suppressed when subjected to bile stress under in vitro conditions. HPLC analysis displayed transformed products from extracellular extract treated samples were comparable to the metabolite standard of the p-cresol degradation pathway. Infrared spectral analysis too showed the spectrum similarity with metabolite standard. Thus, conclusively, intestinal isolates E. faecalis (UTD-1, UTD-2 and UTD-3) might be a promising candidate for mitigating p-cresol detoxification in uremic patients.

Neointimal hyperplasia in the inferior vena cava of adenine-induced chronic kidney disease rats with aortocaval fistulas

The failure of autologous arteriovenous fistulas (AVFs) occurs primarily due to stenosis in the anastomotic site, which is mainly related to the development of neointimal hyperplasia (NIH). Therefore, we conducted a study to establish a novel approach to create aortocaval fistulas (ACFs) in adenine-induced (AD) chronic kidney disease (CKD) rats to study the NIH in the inferior vena cava. Ten adult female rats received a 0.75% adenine-rich diet for 4weeks to induce CKD and underwent ACF surgery. Ten healthy rats served as controls. A 5-10-mm segment of a vein immediately adjacent to that the portion of the vein used for creating the fistula was surgically removed at the time of creating the fistula, and reconstruction of the failed fistula from the same patient was used as controls. ACF was assessed using duplex scans and histopathological analyses. At the end of the experiment, AD rats showed higher serum creatinine and urea nitrogen than those of vehicle-treated rats. Remarkable histological changes in kidney tissues demonstrated successful CKD models. Sections of the ACF in AD rats and veins removed at the time of the reconstruction of the failed fistula of the patient demonstrated that the eccentric neointima formation is irregularly thickened, with several small vessels within a more cellular region of the neointima. Immunohistochemistry demonstrated the presence of myofibroblasts, contractile smooth muscle cells and macrophages within the neointima. Our rat models with ACFs showed typical features of NIH in the formation of fistula stenosis, which can resemble clinical findings in uremic patients.

Apixaban Downregulates Endothelial Inflammatory and Prothrombotic Phenotype in an In Vitro Model of Endothelial Dysfunction in Uremia.

Chronic kidney disease (CKD) associates with inflammatory and prothrombotic phenotypes, resulting in higher cardiovascular risk. Factor Xa displays functions beyond coagulation, exhibiting proinflammatory effects. The aim of the present study was to investigate whether a direct FXa inhibitor protects from the endothelial dysfunction (ED) caused by uremia. Macro (HUVEC) and microvascular (HMEC) endothelial cells (ECs) were exposed to serum from uremic patients or healthy donors, in absence and presence of apixaban (60 ng/ml). We evaluated changes in surface VCAM-1 and ICAM-1, intracellular eNOS, reactive oxygen species (ROS), and von Willebrand Factor (VWF) production by immunofluorescence, reactivity of the extracellular matrix (ECM) towards platelets, and intracellular signaling. ECs exposed to uremic serum triggered dysregulation of all the parameters. Presence of apixaban resulted in decreased expression of VCAM-1 (178 ± 14 to 89 ± 2% on HMEC and 324 ± 71 to 142 ± 25% on HUVEC) and ICAM-1 (388 ± 60 to 111 ± 10% on HMEC and 148 ± 9% to 90 ± 7% on HUVEC); increased eNOS (72 ± 8% to 95 ± 10% on HMEC); normalization of ROS levels (173 ± 21 to 114 ± 13% on HMEC and 165 ± 14 to 127 ± 7% on HUVEC); lower production of VWF (168 ± 14 to 92 ± 4% on HMEC and 151 ± 22 to 99 ± 11% on HUVEC); and decreased platelet adhesion onto ECM (134 ± 22 to 93 ± 23% on HMEC and 161 ± 14 to 117 ± 7% on HUVEC). Apixaban inhibited p38MAPK and p42/44 activation in HUVEC (139 ± 15 to 48 ± 15% and 411 ± 66 to 177 ± 57%, respectively) (p < 0.05 vs control for all parameters). Anti-FXa strategies, such as apixaban, prevented ED caused by the uremic milieu, exhibiting anti-inflammatory and antioxidant properties and modulating the reactivity of the ECM.

Immune Dysfunction in Uremia 2020.

Cardiovascular disease and infections are major causes for the high incidence of morbidity and mortality of patients with chronic kidney disease. Both complications are directly or indirectly associated with disturbed functions or altered apoptotic rates of polymorphonuclear leukocytes, monocytes, lymphocytes, and dendritic cells. Normal responses of immune cells can be reduced, leading to infectious diseases or pre-activated/primed, giving rise to inflammation and subsequently to cardiovascular disease. This review summarizes the impact of kidney dysfunction on the immune system. Renal failure results in disturbed renal metabolic activities with reduced renin, erythropoietin, and vitamin D production, which adversely affects the immune system. Decreased kidney function also leads to reduced glomerular filtration and the retention of uremic toxins. A large number of uremic toxins with detrimental effects on immune cells have been identified. Besides small water-soluble and protein-bound compounds originating from the intestinal microbiome, several molecules in the middle molecular range, e.g., immunoglobulin light chains, retinol-binding protein, the neuropeptides Met-enkephalin and neuropeptide Y, endothelin-1, and the adipokines leptin and resistin, adversely affect immune cells. Posttranslational modifications such as carbamoylation, advanced glycation products, and oxidative modifications contribute to uremic toxicity. Furthermore, high-density lipoprotein from uremic patients has an altered protein profile and thereby loses its anti-inflammatory properties.

Comparative study between drug-coated balloon angioplasty vs plain balloon angioplasty in management of venous stenosis in hemodialysis access circuit

Introduction Juxta-anastomotic venous stenosis is a major concern associated with arteriovenous fistulas, which is mainly a result of neointimal hyperplasia. Although balloon angioplasty remains the cornerstone treatment for vascular access stenosis, the combination of venous anatomy and physiology, with the pre-existing endothelial dysfunction of uremic patients, generally leads to poor mid-term and long-term results. Theoretically, vascular access patency may be optimized by a technology that would both block negative vessel wall remodeling and inhibit fibromuscular hyperplasia. One such approach could be the use of angioplasty with drug-coated balloon (DCB) angioplasty. Patients and methods Within a 10-month period, 80 patients with different types of hemodialysis access stenosis in whom percutaneous transluminal angioplasty (PTA) was indicated were prosTectively, randomized to have either DCB or plain balloon angioplasty (PBA). This study was designed to compare primary patency rates and target lesion revascularization of DCB vs PBA to preserve the patency of the vascular access circuit in patients undergoing hemodialysis after 1 year of follow-up. Results All patients enrolled in the study completed the 1-year follow-up period. Access circuit primary patency results were also significantly in favor of DCB angioplasty (DCB, 287 days, and PBA, 156 days; P=0.04). Target lesion revascularization-free survival was significantly superior in the DCB group according to the Kaplan–Meier survival analysis curve (DCB, 316 days, and PBA, 172 days; P=0.041). There was no statistically significant difference in this subgroup analysis (P>0.1). Conclusion In this two-center study, DCB angioplasty results in improved vessel patency and is superior to plain balloon dilation in the treatment of venous stenoses of failing native or prosthetic arteriovenous shunts used for dialysis access.

Parathyroid Cell Proliferation in Secondary Hyperparathyroidism of Chronic Kidney Disease.

Secondary hyperparathyroidism (SHP) is a common complication of chronic kidney disease (CKD) that correlates with morbidity and mortality in uremic patients. It is characterized by high serum parathyroid hormone (PTH) levels and impaired bone and mineral metabolism. The main mechanisms underlying SHP are increased PTH biosynthesis and secretion as well as increased glandular mass. The mechanisms leading to parathyroid cell proliferation in SHP are not fully understood. Reduced expressions of the receptors for calcium and vitamin D contribute to the disinhibition of parathyroid cell proliferation. Activation of transforming growth factor-α-epidermal growth factor receptor (TGF-α-EGFR), nuclear factor kappa B (NF-kB), and cyclooxygenase 2- prostaglandin E2 (Cox2-PGE2) signaling all correlate with parathyroid cell proliferation, underlining their roles in the development of SHP. In addition, the mammalian target of rapamycin (mTOR) pathway is activated in parathyroid glands of experimental SHP rats. Inhibition of mTOR by rapamycin prevents and corrects the increased parathyroid cell proliferation of SHP. Mice with parathyroid-specific deletion of all miRNAs have a muted increase in serum PTH and fail to increase parathyroid cell proliferation when challenged by CKD, suggesting that miRNA is also necessary for the development of SHP. This review summarizes the current knowledge on the mechanisms of parathyroid cell proliferation in SHP.

Comparative study between sertraline and omega-3 supplementation in the treatment of uremic pruritus in hemodialysis patient

Background: Pruritus in uremic patients decreases the quality of life because of sleep disturbances, depression and anxiety, thus, pruritus remains an important health issue in ESRD patients. Aim of the work:To evaluate the efficacy and safety of sertraline versus omega 3 supplementation in the treatment of uremic pruritus. Patients and Methods:This randomized case control study was conducted on patients with ESRD patients .All studied subjects had been collected from the Al-Azhar hospital [Damietta] Dialysis Center. This study had been carried out on 50 patients divided into: Group [A] : consists of 25patients had been received 50 mg sertraline twice a day for 8 weeks. Group [B]: consists of 25 patients and had been receive 3 gm omega-3 daily. Results: Although pruritus severity decrease significantly in both groups and both scoring systems [P<0.001], the reduction was significantly more in sertraline group [p Conclusion: Omega-3 fatty acids found to be effective in decreasing of uremic pruritus. So, it seems that Omega-3 fatty acids could be used as an efficient drug for treatment of pruritus in uremic patients. The present study showed that low-dose sertraline was effective for antihistamine-refractory uremic pruritus than omeg3 in renal palliative care patients.