Malignant hypertension in a patient with end of stage renal disease (ESRD) treated by renal transplant

Control of hypertension is often a problem in the management of end stage renal disease (ESRD). Multiple modalities of treatment are required to prevent cardiovascular and cerebrovascular mortality and morbidity. These include fluid and salt restriction, multidrug regimes and dialysis. We report a case of young 25 years old patient, admitted with chronic renal failure, complicated by malignant and refractory hypertension, not responding to hemodialysis and antihypertensive agent. During stay in hospital, patient also had intracerebral hemorrhage, fits due to uncontrolled hypertension requiring ventilatory support followed. Renal transplant was considered to be the final therapeutic modality. After gradual recovery, a successful live-related renal transplant was performed. As soon as good graft was established, the blood pressure settled and 4 of the 5 antihypertensives were withdrawn. After 2 weeks, patient was discharged in a stable condition with a total stay of about 2 months.     

Leptin in chronic kidney disease: a link between hematopoiesis,bone metabolism,and nutrition

Anemia, dyslipidemia, malnutrition, together with mineral and bone disorders are common complications in patients with chronic kidney disease (CKD). All are associated with increased risk of mortality. Leptin is a small peptide hormone that is mainly but not exclusively produced in adipose tissue. It is also secreted by normal human osteoblasts, subchondral osteoblasts, placental syncytiotrophoblasts, and the gastric epithelium. Leptin binds to its receptors in the hypothalamus to regulate bone metabolism and food intake. Leptin also has several other important metabolic effects on peripheral tissues, including the liver, skeletal muscle, and bone marrow. Leptin is cleared principally by the kidney. Not surprisingly, serum leptin appears to increase concurrently with declines in the glomerular filtration rate in patients with CKD. A growing body of evidence suggests that leptin might be closely related to hematopoiesis, nutrition, and bone metabolism in CKD patients. Results are conflicting regarding leptin in patients with CKD, in whom both beneficial and detrimental effects on uremia outcome are found. This review elucidates the discovery of leptin and its receptors, changes in serum or plasma leptin levels, the functions of leptin, relationships between leptin and the complications mentioned above, and pharmaceutical interventions in serum leptin levels in patients with CKD.     

Chlamydia pneumoniae,overall and cardiovascular mortality in end-stage renal disease (ESRD)

BACKGROUND: Cross-sectional and retrospective studies suggest that Chlamydia pneumoniae infection may contribute importantly to the high cardiovascular risk of patients with end-stage renal disease (ESRD). METHODS: We investigated the relationship between C. pneumoniae serology and survival and incident fatal cardiovascular events in a cohort of 227 ESRD patients (follow-up of 39 +/- 20 months). RESULTS: On univariate Cox regression analysis patients with anti-C. pneumoniae immunogloblulin A (IgA) titer > or = 1:16 had a significantly higher risk of all-cause and cardiovascular mortality when compared to patients without IgA antibodies. However, after data adjustment for age and smoking, the hazard ratio (HR) decreased substantially and became largely nonsignificant. Adjustments for traditional and nontraditional risk factors further decreased the independent association of IgA anti-C. pneumoniae and these outcomes (all-cause mortality HR, 1.08; 95% CI, 0.68 to 1.72; P = 0.74; cardiovascular mortality HR, 1.07; 95% CI, 0.60 to 1.89; P = 0.83). A similar loss of prognostic power was observed for IgG anti-C. pneumoniae so that in fully adjusted models the HRs were very close to those observed for IgA anti-C. pneumoniae (all-cause mortality HR, 1.13; 95% CI, 0.68 to 1.86, P = 0.64; cardiovascular mortality HR, 1.10; 95% CI, 0.60 to 2.00; P = 0.77). CONCLUSION: C. pneumoniae seropositivity is associated to shorter survival and incident fatal cardiovascular events in patients with ESRD but these associations are in large part attributable to the link between C. pneumoniae and well-established, traditional risk factors. It is highly unlikely that C. pneumoniae infection is a major risk factor in patients with ESRD.     

Is leptin the link between fat and bone mass?

Recently, leptin has emerged as a potential candidate responsible for protective effects of fat on bone tissue. However, it remains difficult to draw a clear picture of leptin effects on bone metabolism because published data are sometimes conflicting or apparently contradictory. Beyond differences in models or experimental procedures, it is tempting to hypothesize that leptin exerts dual effects depending on bone tissue, skeletal maturity, and/or signaling pathway. Early in life, leptin could stimulate bone growth and bone size through direct angiogenic and osteogenic effects on stromal precursor cells. Later, it may decrease bone remodeling in the mature skeleton, when trabecular bone turnover is high, by stimulating osteoprotegerin (OPG) expression. Leptin negative effects on bone formation effected through central nervous system pathway could counterbalance these peripheral and positive effects, the latter being predominant when the blood-brain barrier permeability decreases or the serum leptin level rises above a certain threshold. Thus, the sex-dependent specificity of the relationship between leptin and bone mineral density (BMD) in human studies could be, at least in part, caused by serum leptin levels that are two- to threefold higher in women than in men, independent of adiposity. Although these hypotheses remain highly speculative and require further investigations, existing studies consistently support the role of leptin as a link between fat and bone.     

Pediatric end stage renal disease health-related quality of life differs by modality: a PedsQL ESRD analysis

We previously validated the 34-item PedsQL 3.0 End Stage Renal Disease (ESRD) Module designed to measure pediatric ESRD-specific health-related quality of life (HRQOL) in children and adolescents receiving maintenance dialysis or with a renal transplant. The study reported here was undertaken to assess for potential HRQOL differences between ESRD modality in children with ESRD and their parents using the PedsQL 3.0 ESRD Module. Parents of patients with a renal transplant reported a significantly higher HRQOL for their children than parents of pediatric patients receiving dialysis on all ESRD Module Scales except the Perceived Physical Appearance Scale, with the majority of the effect sizes in the medium range. Pediatric renal transplant patients self-reported comparable HRQOL to pediatric patients receiving dialysis across the ESRD Module Scales, with the exception of the Family and Peer Interaction Scale, in which pediatric renal transplant patients self-reported significantly higher HRQOL than pediatric patients receiving dialysis. Our cross-sectional data suggest that parents of children with ESRD observe a positive impact from renal transplantation on the majority of HRQOL domains compared to dialysis, whereas children self-report generally non-significant small effect size differences in favor of renal transplantation. These findings suggest that the PedsQL ESRD 3.0 Module may be used to identify ESRD- and modality-specific challenges that impact pediatric patient HRQOL. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Dyslipidemia and progression of cardiovascular calcification (CVC) in patients with end-stage renal disease (ESRD)

Dyslipidemia and progression of cardiovascular calcification (CVC) in patients with end-stage renal disease (ESRD). Cardiovascular calcification (CVC) is commonly encountered both in the general population as well as in patients with end-stage renal disease (ESRD). The etiology of CVC in patients with ESRD is multifactorial. Despite that, current debate remains narrowly focused on the role of calcium loading from calcium-based phosphate binders (CBPB) in the pathogenesis and progression of CVC. Yet, the alleged link between these binders and CVC has not been substantiated in well-designed controlled trials. In contrast, the purported role of sevelamer, a non-calcium-based phosphate binder, in slowing the progression of CVC in dialysis patients has attracted widespread attention. The beneficial effect of sevelamer on progression of calcification was thought to be due to lower calcium loading during its use. However, an alternative and possibly more likely mechanism involves sevelamer-induced lowering of LDL cholesterol. In this context, previous studies in individuals with normal renal function have documented amelioration of coronary artery calcification (CAC) with reduction of LDL-cholesterol by treatment with HMG-CoA reductase inhibitors (statins). Given that CAC is a well-accepted marker of atherosclerosis, and that high plasma cholesterol concentration is one of the main risk factors for atherosclerosis, then it is not unreasonable to suspect that CAC may be halted or even reversed by lowering of LDL cholesterol level with statin therapy. Unfortunately, the effect of lowering the LDL-cholesterol level on CAC has not been studied in patients with ESRD. Therefore, conclusions about this important topic should await the results of well-designed clinical studies that control for all factors potentially implicated in the CVC burden of patients with ESRD. In this review, I will discuss the role of various potential mechanisms involved in the pathogenesis of CVC in patients with ESRD, and emphasize the role of dyslipidemia and its treatment in this important clinical entity.     

Leptin: a potential mediator for protective effects of fat mass on bone tissue

Body weight is among the most powerful predictors of bone status, and adipose tissue plays a substantial role in weight-related protective effects on bone. An understanding of the mechanisms underlying the relation between adipose tissue and bone may open up new perspectives for treatment. Leptin, which is known to regulate appetite and energy expenditures, may also contribute to mediate the effects of fat mass on bone. Although reported data are somewhat conflicting, there is some evidence that leptin may decrease bone formation via a central nervous effect and may stimulate both bone formation and bone resorption via direct peripheral effects on stromal precursor cells. The net result of these central and peripheral effects may depend on serum leptin levels and blood-brain barrier permeability, of which the first increase and the second decrease as obesity develops. Further work is needed to improve our understanding of these effects.     

Chemerin rs17173608 and vaspin rs2236242 gene variants on the risk of end stage renal disease (ESRD) and correlation with plasma malondialdehyde (MDA) level

Introduction: End-stage renal disease (ESRD) is associated with critical kidney illness that seriously affects the lifespan. Genetic factors and oxidative stress could play critical role in the development of ESRD. We assessed the association between chemerin rs17173608 T/G and vaspin rs2236242 T/A genes variants with the risk of ESRD and their correlation with plasma malondialdehyde (MDA) level.

Materials and methods: In a case-control study, 131 gender and age-matched unrelated healthy controls and 110 ESRD patients were enrolled. The chemerin rs17173608 T/G and vaspin rs2236242 T/A were detected by Tetra primer-amplification refractory mutation system-polymerase chain reaction (T-ARMS-PCR). The MDA concentration was determined by HPLC.

Results: Our findings for the first time revealed that in codominant genetic model (T/G vs. T/T genotype), the T/G genotype of chemerin gene significantly had a protective role against ESRD susceptibility. Also, in the presence of chemerin G allele, the risk of ESRD decreased by 0.79-fold (p?=?.048) in Kurdish population of Iran. The MDA serum levels in ESRD patients carrying the chemerin T/G?+?G/G genotype of rs17173608 T/G and also in carriers of A/A?+?T/A genotype of vaspin rs2236242 T/A were significantly higher compared to those in control subjects. The overall distribution of vaspin rs2236242 T/A genotypes and alleles comparing ESRD patients and healthy subjects were not statistically significant.

Conclusion: We found that the G allele of chemerin rs17173608 compared to T allele decreased the risk of ESRD, and there was a significant association between chemerin and vaspin variants with plasma MDA level in a sample of the Iranian population.     

Pyocystis, pyonephrosis and perinephric abscess in end stage renal disease

We report 8 patients with end stage renal disease on maintenance hemodialysis who had pyocystis, pyonephrosis or a perinephric abscess. Delay in diagnosis was frequent because the urine-deprived bladder and kidneys were dismissed as potential sites of infection. Treatment of pyocystis with bladder irrigations often was successful and obviated cystectomy. Pyonephrosis or perinephric abscess was a more serious problem and required unilateral nephrectomy.     

腹膜透析联合血液透析对终末期肾脏疾病患者心血管病变的改善作用

目的通过对腹膜透析联合血液透析(peritoneal dialysis combined with hemodialysis,PHD)后与联合治疗前相关指标进行比较,探讨联合治疗对终末期肾脏疾病(end stage renal disease,ESRD)患者心血管病变的改善作用。方法回顾性分析济宁医学院附属医院肾内科14例腹膜透析(peritoneal dialysis,PD)治疗不充分的ESRD患者,改用PHD治疗后的临床疗效。随访观察患者的一般状况、临床表现、营养状态,收集其治疗前后生化指标、甲状旁腺素、β_2微球蛋白(β_2-microglobulin,β_2-MG)、颈动脉内中膜厚度(carotid intima media thickness,CIMT)、收缩压、舒张压、左室射血分数、B型钠尿肽(B type natriuretic peptide,BNP)进行分析。结果经过PHD治疗后患者饮食好转,恶心、呕吐等消化道症状消失,曾反复心力衰竭的3例患者行PHD治疗后未再出现,皮肤瘙痒及不宁腿症状明显减轻。PHD前与PHD治疗后比较,血磷:(1.76±0.41)mmol/L与(1.48±0.28)mmol/L,P0.05;甲状旁腺素:(367.93±166.66)ng/L与(237.07±76.21)ng/L,P0.05;BNP:(1 521.7±701.0)μg/L与(712.1±535.0)μg/L,P0.01;左室射血分数:(49.7±3.1)%与(52.2±1.8)%,P0.05;颈动脉内中膜厚度:(1.65±0.36)mm与(1.72±0.33)mm,P0.05,PHD治疗后较PHD前无明显改变。结论 PHD能减轻患者的临床症状,改善患者的营养状态,降低血磷,减轻继发性甲状旁腺功能亢进,延缓动脉硬化进展,可作为一种新的肾脏替代治疗模式在临床推广。     

Acquired renal cystic disease in the end stage kidney: urological implications

A unique form of acquired renal cystic disease occurs commonly in the end stage kidneys of patients with chronic renal failure. Recent experience with 3 cases of acquired renal cystic disease has made us aware that the condition has significant urological implications. The pathogenesis of this disease is unknown but may be related to tubular obstruction, ischemia or the accumulation of toxic products. The diagnosis of acquired renal cystic disease is established by either ultrasound or computerized tomography, both of which demonstrate bilateral multiple small cysts scattered throughout the cortex and medulla of the contracted end stage kidney. Acquired renal cystic disease usually is asymptomatic but may be associated with either hemorrhage or neoplasia. Autopsy studies have revealed renal tumors in up to 45 per cent of the patients with acquired renal cystic disease. These tumors usually are small but our case 3 was a renal cell carcinoma that measured 4 cm. in diameter. Also, there have been other recent reports of large tumors and deaths of metastatic renal carcinoma in patients with acquired renal cystic disease. Patients with chronic renal failure should undergo periodic examination of the native kidneys by either ultrasound or computerized tomography. It may be difficult to distinguish benign from malignant lesions radiologically, and nephrectomy may be indicated when the diagnosis is uncertain.     

Discrepancy in results between spine and hip scans of a woman with end stage renal disease.

Conditions and artifacts such as aortic calcifications, osteophytes, hip prostheses, and metallic objects can affect the results of dual X-ray absorptiometry scans of the spine and hip. Abdominal surgery often entails the use of metal sutures causing subtle artifacts near or over the lumbar spine resulting in inaccurate bone mineral density (BMD) measurements. We herein report a case of a woman whose spine BMD appeared normal while her hip BMD was > -3.5 SDs. Although the abdominal artifacts create some uncertainty in the diagnosis, renal osteodystrophy is suspect owing to the patient's renal history. This case demonstrates the importance of acquiring scans at two or more sites, closely evaluating scans for artifacts, and obtaining the patient's medical history.     

Racial differences in chronic kidney disease (CKD) and end-stage renal disease (ESRD) in the United States: a social and economic dilemma

Chronic kidney disease (CKD), defined as an eGFR < 60 ml/min/1.73 m2, affects up to 25% of the United States population. In addition, it is estimated that approximately 6% of the population have early evidence of CKD and will likely progress to end stage renal disease (ESRD) in the near future. Further, ESRD is more common in many ethnic minorities, with African-Americans having the highest rates of treated ESRD, closely followed by Hispanic Americans, when compared to non- Hispanic White persons. Although African-Americans with CKD are more likely to die than non-Hispanic White persons with CKD, these trends reverse once progression to ESRD is established. The reasons for the disparities in the prevalence and incidence of CKD, ESRD, and mortality are unclear, but likely involve a complex interaction of socioeconomic, environmental and genetic factors. This review highlights current data pertaining to the social and economic impact of ethnic differences in the prevalence and incidence of CKD and ESRD in the United Stated. It is hoped that highlighting the current trend of kidney related health disparities will not only lead to an improved understanding of these issues, but also more informed research agendas, that are ultimately aimed at alleviating ethnic differences in kidney health outcomes.     

Is oxidative stress implicated in high bone turnover in end-stage renal disease (ESRD)?

Sir, End stage renal disease (ESRD) is a condition in which oxidativestress is much enhanced and implicated in a variety of uremiccomplications [1,2]. Oxidative stress influences bone turnover     

Abdominal catastrophe in a 43-year-old female with end stage renal disease

A 43-year-old female with end-stage renal disease secondary to focal segmental glomerulosclerosis was admitted to the hospital for shortness of breath after missing hemodialysis. On admission, the patient was noted to have painful skin lesions consistent with calciphylaxis on biopsy. While undergoing aggressive wound care, she developed altered mental status and was found to be septic and started empirically on broad-spectrum antibiotics. The patient was intubated on day 4 of admission owing to worsening mental status and acidemia. She had persistent positive blood cultures throughout her hospitalization despite appropriate antibiotic therapy. On day 25 of admission, the patient was found to have abdominal distension. A radiograph revealed intra-abdominal free air, and the patient was taken to the operating room where she was found to have perforated necrotic bowel. The patient expired on day 26 of admission. An autopsy revealed calciphylaxis within the gut wall and within the dura of the central nervous system. While typically a disorder of subcutaneous tissue, calciphylaxis can affect internal organs, which in this case resulted in a catastrophic outcome.