Treatment strategies of the thromboembolic risk in kidney failure patients with atrial fibrillation.

The incidence and prevalence of atrial fibrillation (AF) in patients affected by kidney failure, i.e. glomerular filtration rate <15 ml/min/1.73 m2, is high and probably underestimated. Numerous uncertainties remain regarding how to prevent thromboembolic events in this population because both cardiology and nephrology guidelines do not provide clear recommendations. The efficacy and safety of oral anticoagulant therapy (OAC) in preventing thromboembolism in patients with kidney failure and AF has not been demonstrated for either vitamin K antagonists (VKAs) or direct anticoagulants (DOACs). Moreover, it remains unclear which is more effective and safer, because estimated creatinine clearance <25-30 ml/min was an exclusion criterion in the randomized controlled trials (RCTs). Three RCTs comparing DOACs and VKAs in kidney failure failed to reach the primary endpoint, as they were underpowered. The left atrial appendage is the main source of thromboembolism in the presence of AF. Left atrial appendage closure (LAAC) has recently been proposed as an alternative to OAC. RCTs comparing the efficacy and safety of LAAC versus OAC in kidney failure were terminated prematurely due to recruitment failure. A recent prospective study showed a reduction in thromboembolic events in haemodialysis patients with AF and undergoing LAAC compared with patients taking or not taking OAC. We review current treatment standards and discuss recent developments in managing the thromboembolic risk in kidney failure patients with AF. The importance of shared decision-making with the multidisciplinary team and the patient to consider individual risks and benefits of each treatment option is underlined.

Home-based exercise in patients on maintenance dialysis: a systematic review and meta-analysis of randomized clinical trials.

BACKGROUND: The impact of home-based exercise on physical performance and quality of life (QoL) in patients on maintenance dialysis has not yet been fully established. METHODS: We searched four large electronic databases to identify randomized controlled trials (RCTs) reporting the impact of home-based exercise interventions vs. usual care or intradialytic exercise interventions, on physical performance and QoL in patients on dialysis. The meta-analysis was performed using fixed effects modeling. RESULTS: We included 12 unique RCTs involving 791 patients of various ages on maintenance dialysis. Home-based exercise interventions were associated with an improvement of walking speed at the 6 Minutes Walking Test [6MWT; nine RCTs; pooled weighted mean differences (WMD): 33.7 m, 95% confidence interval (CI) 22.8-44.5; P < 0.001; I2 = 0%) and in aerobic capacity as assessed by the peak oxygen consumption (VO2 peak; 3 RCTs; pooled WMD: 2.04 ml/kg/min, 95% CI 0.25-3.83; P = 0.03; I2 = 0%). They were also associated with improved QoL, as assessed by the Short Form (36) Health (SF-36) score. Stratifying the RCTs by control groups, no significant difference was found between home-based exercise and intradialytic exercise interventions. Funnel plots did not reveal any significant publication bias. CONCLUSIONS: Our systematic review and meta-analysis showed that home-based exercise interventions for 3-6 months were associated with significant improvements in physical performance in patients on maintenance dialysis. However, further RCTs with a longer follow-up should be conducted to assess the safety, adherence, feasibility, and effects on QoL of home-based exercise programs in dialysis patients.

Post-acute COVID-19 syndrome and kidney diseases: what do we know?

COVID-19, a disease caused by a novel coronavirus (SARS-CoV-2), is a major global threat that has turned into a pandemic. Despite the emergence of multiple vaccination alternatives and developing therapeutic options, dramatic short- and long-term clinical outcomes have been recorded with more than 250 million infected people and over 5 million deaths as of November 2021. COVID-19 presents various respiratory, cardiovascular, neuropsychiatric, musculoskeletal and kidney features during the acute phase; nevertheless, renal involvement in the post-infection period has recently been emphasized. The present review aims to evaluate the growing literature on kidney involvement in the SARS-CoV-2 infection along with clinical features reported both in the acute phase of the infection and in the post-acute COVID-19 period by assessing potential pathophysiological frameworks explaining such conditions. Chronic kidney disease and development of acute kidney injury (AKI) in the course of initial hospitalization are associated with high mortality and morbidity rates. Moreover, growing evidence suggests a decline in renal function in the 6-to-12-month follow-up period even in patients without any signs of AKI during the acute phase. Despite such concerns there are no guidelines regulating the follow-up period or therapeutic alternatives for such patient population. In conclusion, the burden of COVID-19 on the kidney is yet to be determined. Future prospective large scale studies are needed with long follow-up periods assessing kidney involvement via multiple parameters such as biopsy studies, urinalysis, measurement of serum creatinine and cystatin C, directly measured glomerular filtration rate, and assessment of tubular function via urinary ß2-microglobulin measurements.

A call to optimize haemodialysis vascular access care in healthcare disrupted by COVID-19 pandemic.

The COVID-19 pandemic has resulted in major disruption to the delivery of both routine and urgent healthcare needs in many institutions across the globe. Vascular access (VA) for haemodalysis (HD) is considered the patient's lifeline and its maintenance is essential for the continuation of a life saving treatment. Prior to the COVID-19 pandemic, the provision of VA for dialysis was already constrained. Throughout the pandemic, inevitably, many patients with chronic kidney disease (CKD) have not received timely intervention for VA care. This could have a detrimental impact on dialysis patient outcomes in the near future and needs to be addressed urgently. Many societies have issued prioritisation to allow rationing based on clinical risk, mainly according to estimated urgency and need for treatment. The recommendations recently proposed by the European and American Vascular Societies in the COVID-19 pandemic era regarding the triage of various vascular operations into urgent, emergent and elective are debatable. VA creation and interventions maintain the lifeline of complex HD patients, and the indication for surgery and other interventions warrants patient-specific clinical judgement and pathways. Keeping the use of central venous catheters at a minimum, with the goal of creating the right access, in the right patient, at the right time, and for the right reasons, is mandatory. These strategies may require local modifications. Risk assessments may need specific "renal pathways" to be developed rather than applying standard surgical risk stratification. In conclusion, in order to recover from the second wave of COVID-19 and prepare for further phases, the provision of the best dialysis access, including peritoneal dialysis, will require working closely with the multidisciplinary team involved in the assessment, creation, cannulation, surveillance, maintenance, and salvage of definitive access.

Coronary artery disease in dialysis patients: evidence synthesis, controversies and proposed management strategies.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality among patients with end-stage renal disease (ESRD). Clustering of traditional atherosclerotic and non-traditional risk factors drive the excess rates of coronary and non-coronary CVD in this population. The incidence, severity and mortality of coronary artery disease (CAD) as well as the number of complications of its therapy is higher in dialysis patients than in non-chronic kidney disease patients. Given the lack of randomized clinical trial evidence in this population, current practice is informed by observational data with a significant potential for bias. Furthermore, guidelines lack any recommendation for these patients or extrapolate them from trials performed in non-dialysis patients. Patients with ESRD are more likely to be asymptomatic, posing a challenge to the correct identification of CAD, which is essential for appropriate risk stratification and management. This may lead to "therapeutic nihilism", which has been associated with worse outcomes. Here, the ERA-EDTA EUDIAL Working Group reviews the diagnostic work-up and therapy of chronic coronary syndromes, unstable angina/non-ST elevation and ST-elevation myocardial infarction in dialysis patients, outlining unclear issues and controversies, discussing recent evidence, and proposing management strategies. Indications of antiplatelet and anticoagulant therapies, percutaneous coronary intervention and coronary artery bypass grafting are discussed. The issue of the interaction between dialysis session and myocardial damage is also addressed.

What volume to choose to assess online Kt/V?

INTRODUCTION: Urea distribution volume (V) can be assessed in different ways, among them the anthropometric Watson Volume (VW). However, many studies have shown that VW does not coincide with V and that the latter can be more accurately estimated with other methods. The present multicentre study was designed to answer the question: what V to choose to assess online Kt/V? MATERIALS AND METHODS: Pre- and postdialysis blood urea nitrogen concentrations and the usual input data set for urea kinetic modelling were obtained for a single dialysis session in 201 Caucasian patients treated in 9 Italian dialysis units. Only dialysis machines measuring ionic dialysance (ID) were utilized. ID reflects very accurately the mean effective dialyser urea clearance (Kd). Six different V values were obtained: the first one was VW; the second one was computed from the equation established by the HEMO Study to predict the single pool-adjusted modelled V from VW (VH) (Daugirdas JT et al. KI 64: 1108, 2003); the others were estimated kinetically as: 1. V_ID, in which ID is direct input in the in the double pool variable volume (dpVV) calculation by means of the Solute-solver software; 2. V_Kd, in which the estimated Kd is direct input in the dpVV calculation by means of the Solute-solver software; 3. V_KTV, in which V is calculated by means of the second generation Daugirdas equation; 4. V_SPEEDY, in which ID is direct input in the dpVV calculation by means of the SPEEDY software able to provide results quite similar to those provided by Solute-solver. RESULTS: Mean± SD of the main data are reported: measured ID was 190.6 ± 29.6 mL/min, estimated Kd was 211.6 ± 29.0 mL/min. The relationship between paired data was poor (R2 = 0.34) and their difference at the Bland-Altman plot was large (21 ± 27 mL/min). VW was 35.3 ± 6.3 L, VH 29.5 ± 5.5, V_ID 28.99 ± 7.6 L, V_SPEEDY 29.4 ± 7.6 L, V_KTV 29.7 ± 7.0 L. The mean ratio VW/V_ID was 1.22, (i.e. VW overestimated V_ID by about 22%). The mean ratio VH/V_ID was 1.02 (i.e. VH overestimated V_ID by only 2%). The relationship between paired data of V_ID and VW was poor (R2 = 0.48) and their mean difference at the Bland-Altman plot was very large (- 6.39 ± 5.59 L). The relationship between paired data of V_ID and VH was poor (R2 = 47) and their mean difference was small but with a large SD (- 0.59 ± 5.53 L). The relationship between paired data of V_ID and V_SPEEDY was excellent (R2 = 0.993) and their mean difference at the Bland-Altman plot was very small (- 0.54 ± 0.64 L). The relationship between paired data of V_ID and V_KTV was excellent (R2 = 0.985) and their mean difference at the Bland-Altman plot was small (- 0.85 ± 1.06 L). CONCLUSIONS: V_ID can be considered the reference method to estimate the modelled V and then the first choice to assess Kt/V. V_SPEEDY is a valuable alternative to V_ID. V_KTV can be utilized in the daily practice, taking also into account its simple way of calculation. VW is not advisable because it leads to underestimation of Kt/V by about 20%.

[Membranoproliferative glomerulonephritis with relapsing episodes of acute kidney injury in the Schnitzler syndrome].

The Schnitzler syndrome (SS) is a rare and underdiagnosed entity that associates a chronic urticarial rash, monoclonal IgM (or sometimes IgG) gammopathy and signs and symptoms of systemic inflammation. During the past 45 years the SS has evolved from an elusive, little-known disorder to the paradigm of a late-onset auto-inflammatory acquired syndrome. Though there is no definite proof of its precise pathogenesis, it should be considered as an acquired disease involving abnormal stimulation of the innate immune system, which can be reversed by the interleukin 1 (IL-1) receptor antagonist anakinra. Here we describe the case of a 56-year-old male Caucasian patient affected by SS and hospitalized several times in our unit because of relapsing episodes of acute kidney injury. He underwent an ultrasound-guided percutaneous kidney biopsy in September 2012, which showed the histologic picture of type I membranoproliferative glomerulonephritis. He has undergone conventional therapies, including nonsteroidal anti-inflammatory drugs, steroids and immunosuppressive drugs; more recently, the IL-1 receptor antagonist anakinra has been prescribed, with striking clinical improvement. Although the literature regarding kidney involvement in the SS is lacking, it can however be so severe, as in the case reported here, to lead us to recommend the systematic search of nephropathy markers in the SS.

The function of the parathyroid oxyphil cells in uremia: still a mystery?

Parathyroid glands of young adults consist primarily of chief cells. However, with age or after excessive functional stress, another cell type increases progressively-the oxyphil cell. There is evidence for a chief-to-oxyphil cell transdifferentiation in chronic kidney disease. The latter may represent a defense mechanism, transforming the actively secreting chief cells to a less actively secreting cell type. However, even if this strategy is able to delay the development of secondary hyperparathyroidism, it cannot prevent it.

Is incremental hemodialysis ready to return on the scene? From empiricism to kinetic modelling.

Most people who make the transition to maintenance dialysis therapy are treated with a fixed dose thrice-weekly hemodialysis regimen without considering their residual kidney function (RKF). The RKF provides effective and naturally continuous clearance of both small and middle molecules, plays a major role in metabolic homeostasis, nutritional status, and cardiovascular health, and aids in fluid management. The RKF is associated with better patient survival and greater health-related quality of life, although these effects may be confounded by patient comorbidities. Preservation of the RKF requires a careful approach, including regular monitoring, avoidance of nephrotoxins, gentle control of blood pressure to avoid intradialytic hypotension, and an individualized dialysis prescription including the consideration of incremental hemodialysis. There is currently no standardized method for applying incremental hemodialysis in practice. Infrequent (once- to twice-weekly) hemodialysis regimens are often used arbitrarily, without knowing which patients would benefit the most from them or how to escalate the dialysis dose as RKF declines over time. The recently heightened interest in incremental hemodialysis has been hindered by the current limitations of the urea kinetic models (UKM) which tend to overestimate the dialysis dose required in the presence of substantial RKF. This is due to an erroneous extrapolation of the equivalence between renal urea clearance (Kru) and dialyser urea clearance (Kd), correctly assumed by the UKM, to the clinical domain. In this context, each ml/min of Kd clears the urea from the blood just as 1 ml/min of Kru does. By no means should such kinetic equivalence imply that 1 ml/min of Kd is clinically equivalent to 1 ml/min of urea clearance provided by the native kidneys. A recent paper by Casino and Basile suggested a variable target model (VTM) as opposed to the fixed model, because the VTM gives more clinical weight to the RKF and allows less frequent hemodialysis treatments at lower RKF. The potentially important clinical and financial implications of incremental hemodialysis render it highly promising and warrant randomized controlled trials.

Preoperative assessment and planning of haemodialysis vascular access.

Effective haemodialysis (HD) requires a reliable vascular access (VA). Clinical practice guidelines strongly recommend the arteriovenous fistula (AVF) as the preferred VA in HD patients. The creation of an AVF should be promoted in all eligible patients who choose HD, as it improves outcomes and reduces costs when compared with central venous catheters. Fistula eligibility is a 'work in progress'. Three steps in order to increase the pool of eligible patients can be individualized: (i) process of care, which includes three fundamental items: the VA team, early VA education and timely VA surgery referral; (ii) preoperative evaluation; (iii) surgical strategy. Nephrologists should be able to play a leading and coordinating role of the VA team. They should design a plan that identifies a sequence of options that can be used to provide adequate renal replacement therapy throughout the life span of every end-stage renal disease patient. The main points of this strategy are (i) early vascular education, in which a 'save the vein program' should always be implemented; (ii) timely VA surgery referral and preoperative evaluation: careful examination of arterial and venous beds is mandatory before VA placement; physical examination in addition to colour Doppler ultrasound mapping improves AVF outcomes; (iii) surgical strategy: a successful VA strategy must take into account vascular anatomy, clinical factors and prognosis.

[Must we always treat hyperkalaemia?]. / Dobbiamo trattare sempre l'iperpotassiemia?

Pseudohyperkalaemia that occurs in conditions with raised platelet counts is caused by an in vitro rise of the serum potassium concentration during whole blood coagulation together with lysis of platelets and other cellular components, in the presence of normal renal function and plasma potassium levels. Here, we report the case of a 66-year-old man presenting a myeloproliferative disorder with thrombocythaemia. His serum potassium level was 6.4 mmol/L in the presence of normal renal function (creatinine clearance 78 mL/min) and a normal acid-base balance. Pseudohyperkalaemia in thrombocythaemia was suspected. Our suspicion was confirmed over the following three days by measuring potassium level in both a lithium heparin specimen tube (plasma sample) and in the serum. A clear-cut difference between serum potassium levels (mean 6.27 mmol/L) and plasma potassium levels (mean 4.10 mmol/L) was found. In conclusion, the aim of the present case report is to increase the awareness of the existence of pseudohyperkalaemia occurring in diseases that cause increased platelet counts in order to reduce the risk of potentially harmful treatment.

Fibromuscular dysplasia of renal arteries presenting with bilateral renal infarction in a young man.

Fibromuscular dysplasia (FMD) describes a group of conditions which cause nonatheromatous arterial stenoses, most commonly of the renal and carotid arteries, typically in young women. We report the case of a previously healthy 43-year-old white man presenting with acute bilateral flank pain. The pain was more severe on the left side. Initially treated for ureteral colic, he was transferred to the nephrology unit upon recognition of a rising serum creatinine. He was found to have FMD of bilateral renal arteries with resultant infarctions in both kidneys. He was treated with intravenous heparin and, then, warfarin at discharge. At a 16-month review, the patient remained pain-free with normal renal function and with antiplatelet and dual antihypertensive therapy. In conclusion, renal infarction complicating FMD is rare, with most cases involving causative cardiovascular risk factors, including coagulopathy, ischemic heart disease, atrial fibrillation or structural cardiac abnormalities, none of which was present in this case. What makes this case interesting are the clinically significant bilateral renal infarctions due to atypical asymmetric FMD in both kidneys in a young man.

Predictors of haemoglobin levels and resistance to erythropoiesis-stimulating agents in patients treated with low-flux haemodialysis, haemofiltration and haemodiafiltration: results of a multicentre randomized and controlled trial.

BACKGROUND: Predictors of haemoglobin (Hb) levels and resistance to erythropoiesis-stimulating agents (ESAs) in dialysis patients have not yet been clearly defined. Some mainly uncontrolled studies suggest that online haemodiafiltration (HDF) may have a beneficial effect on Hb, whereas no data are available concerning online haemofiltration (HF). The objectives of this study were to evaluate the effects of convective treatments (CTs) on Hb levels and ESA resistance in comparison with low-flux haemodialysis (HD) and to evaluate the predictors of these outcomes. METHODS: Primary multivariate analysis was made of a pre-specified secondary outcome of a multicentre, open-label, randomized controlled study in which 146 chronic HD patients from 27 Italian centres were randomly assigned to HD (70 patients) or CTs: online pre-dilution HF (36 patients) or online pre-dilution HDF (40 patients). RESULTS: CTs did not affect Hb levels (P = 0.596) or ESA resistance (P = 0.984). Hb correlated with polycystic kidney disease (P = 0.001), C-reactive protein (P = 0.025), ferritin (P = 0.018), ESA dose (P < 0.001) and total cholesterol (P = 0.021). The participating centres were the main source of Hb variability (partial eta(2) 0.313, P < 0.001). ESA resistance directly correlated with serum ferritin (P = 0.030) and beta2 microglobulin (P = 0.065); participating centres were again a major source of variance (partial eta(2) 0.367, P < 0.001). Transferrin saturation did not predict either outcome variables (P = 0.277 and P = 0.170). CONCLUSIONS: In comparison with low-flux HD, CTs did not significantly improve Hb levels or ESA resistance. The main sources of variability were participating centres, ESA dose and the underlying disease.

The mckittrick-wheelock syndrome: a rare cause of severe hydroelectrolyte disorders and acute renal failure.

The McKittrick-Wheelock syndrome is a rare cause of severe hydroelectrolyte disorders and fluid depletion as a result of rectal tumor hypersecretion, which can lead to acute renal failure. We report the case of a 70-year-old female who presented with hyponatremia, hypokalemia, hypochloremia, and acute renal failure, due to a watery, mucinous diarrhea. A large rectal villous adenoma was discovered on ileocolonoscopy, and definitive management was achieved by removal of the tumor. In conclusion, reversal of the biochemical derangement is the cornerstone of successful management of the McKittrick-Wheelock syndrome. Then, immediate surgical resection of the tumor is the treatment of choice.

[A case of drug-induced syndrome of inappropriate secretion of antidiuretic hormone]. / Un caso di sindrome da inappropriata secrezione di ormone antidiuretico indotta da farmaci.

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is characterized by hyponatremia, plasma hypo-osmolality, a urine sodium concentration >30-40 mmol/L, normal acid-base balance, a normal plasma potassium concentration and, frequently, hypouricemia. There are different types of SIADH: idiopathic, iatrogenic, and forms caused by central nervous system or lung disorders, neoplasia and major surgical interventions. Drug-induced SIADH is becoming the most frequent cause of hyponatremia encountered in clinical practice. Here we report the case of a 60-year-old man in a coma (I-II) and with very severe hyponatremia (99 mmol/L) due to SIADH induced by fluphenazine and amitriptyline, which he had been taking since many years as antidepressant drugs. SIADH became very quickly more severe due to the recent administration of cisplatin. There was rapid improvement of the clinical symptoms after withdrawal of the drugs involved and correction of hyponatremia. In conclusion, in rare cases like the present one hyponatremia related to SIADH may be so severe as to represent a true clinical emergency. The administration of drugs known to cause hyponatremia should be avoided, if possible; otherwise, very careful monitoring of the plasma sodium concentration is mandatory to avoid severe neurological complications which may lead to the death of the patient.

Cinacalcet is effective in relapses of secondary hyperparathyroidism after parathyroidectomy.

BACKGROUND: Relapses of secondary hyperparathyroidism (SHPTH) after parathyroidectomy (PTx) in haemodialysis patients are relatively frequent. Calcimimetics (cinacalcet HCl) offer a new therapeutic opportunity for their treatment. However, no data about the treatment with cinacalcet of relapses of SHPTH after PTx are available in literature. The aim of this single-centre prospective study was to evaluate the therapeutic efficacy of cinacalcet in this high-risk category of patients. METHODS: Twelve haemodialysis patients of our Dialysis Unit had a relapse of SHPTH after PTx, defined as serum levels of immunoreactive intact parathyroid hormone (iPTH)>300 pg/ml. They were stratified into a treatment group (the six patients having the highest serum levels of iPTH) and a control group (the remaining six patients): the former were treated for 6 months with a dose of cinacalcet ranging from 30 mg every other day to 60 mg a day; the latter continued to be administered the conventional treatment. Serum levels of albumin, iPTH, calcium (Ca), phosphate (P) and alkaline phosphatase were determined monthly. The treatment group included four cases of nodular hyperplasia and two cases of carcinoma of parathyroid glands, whereas the control group included four cases of nodular hyperplasia and two cases of diffuse hyperplasia. RESULTS: At the start of the study, the six patients treated with cinacalcet showed a more severe picture of biochemical abnormalities when compared with the control patients. After 6 months of treatment, a statistically significant reduction in the serum levels of iPTH, Ca, P and CaxP product was obtained only in the patients treated with cinacalcet. Symptomatic episodes of hypocalcaemia (serum Ca<7.0 mg/dl) were observed in three patients of this group. The six patients undergoing the conventional treatment showed at 6 months a not significant decrease in the mean serum levels of iPTH and a not significant increase in the mean serum levels of Ca, P and CaxP product, when compared with the baseline values. CONCLUSIONS: Our single-centre prospective study, even though small and of short duration, shows that cinacalcet is effective also in controlling relapses of SHPTH after PTx, thus representing a solid, and sometimes unique, therapeutic opportunity for this high-risk category of patients.

End-stage renal disease in leprosy.

BACKGROUND: Leprosy or Hansen's disease (HAD) undoubtedly remains an emergency in certain countries. It is an ancient deforming disease caused by Mycobacterium leprae. The countries with the highest endemic leprosy rate in 2000 were Brazil, India and Madagascar. In Italy, the old epidemic has been defeated and there are approximately 400 patients under constant monitoring with three to four new cases per year involving Italian residents. The kidney is one of the target organs during the splanchnic localization of leprosy. The histopathological renal lesion spectrum includes glomerulonephritis (GN), renal amyloidosis (RA) and interstitial nephritis (IN). Both proteinuria and chronic renal failure are the main clinical expressions of renal damage in leprosy. To the best of our knowledge, very little is reported concerning end-stage renal disease (ESRD) in leprosy patients both in the most important national and international renal registries and in the available literature. This study aimed to report the long-term experience of our department in this field. METHODS: To achieve this, we analyzed retrospectively the HAD Center (Gioia del Colle) database at ourhospital. RESULTS: Eight leprosy patients were dialyzed from 1980 to June 2003 (six males and two females), with a mean age of 61.0+/-8.9 SD yrs (range: 51-76) and a mean HAD duration of 36.1+/-5.1 yrs. The first clinical nephropathymanifestations were non-nephrotic proteinuria associated with chronic renal failure in four patients, and nephrotic proteinuria in four patients. Kidney biopsies performed in three patients showed two had RA, and one had IN. Two patients were treated initially by peritoneal dialysis; they were then switched to hemodialysis (HD) after 3 and 10 months because of recurrent peritonitis. HD treatment lasted 40.6+/-31.4 months (range: 9-101). Six patients died, one due to hyperkalemia, one because of a technical dialysis accident, and the remainder due to causes unrelated to the dialysis treatment. Two patients are still alive, treated with HD for 17 and 44 months. CONCLUSIONS: Uremia represents a late complication of leprosy and has a multifactorial genesis, although RA is among the most frequent causes, conventional bicarbonate HD appears to offer good results in the treatment of uremia in leprosy patients.

The natural history of autogenous radio-cephalic wrist arteriovenous fistulas of haemodialysis patients: a prospective observational study.

BACKGROUND: Clinical practice guidelines have supported vascular access surveillance programmes on the premise that the natural history of the vascular access will be altered by radiological or surgical interventions after vascular access dysfunction is detected. The primary objective of this study was to assess the actual risk of thrombosis of autogenous radio-cephalic (RC) wrist arteriovenous fistulas (AVFs) without any pre-emptive interventions. METHODS: We enrolled 52 randomly selected adult Caucasian prevalent haemodialysis (HD) patients, all with autogenous RC wrist AVFs, into this prospective, observational study aimed to follow the natural history of their AVFs for 4 years. The protocol prescribed avoiding any surgical or interventional radiological procedures until access failure (AVF thrombosis or a vascular access not assuring a single-pool Kt/V > or =1.2). The subjects underwent yearly assessments of vascular access blood flow rate by means of a saline ultrasound dilution method. RESULTS: All failures of vascular access were due to AVF thrombosis; none were attributed to an inadequacy of the dialysis dose. AVF thrombosis occurred in nine cases; a rate of 0.043 AVF thrombosis per patient-year at risk. A receiver operating characteristic curve, evaluating the diagnostic accuracy of baseline vascular access blood flow rate values in predicting AVF failure, showed an under-the-curve area of 0.82+/-0.05 SD (P = 0.01). The value of vascular access blood flow rate, identified as a predictor of AVF failure, was <700 ml/min with an 88.9% sensitivity and 68.6% specificity. When subdividing the population of AVFs into two groups according to the baseline vascular access blood flow rates, two out of the nine thromboses occurred among the AVFs that had baseline blood flow rates >700 ml/min (n = 31), whereas seven occurred among the AVFs that had baseline blood flow rates <700 ml/min (n = 21). The 4 year cumulative actuarial survival was 74.36 and 20.80%, respectively (log-rank test, P = 0.04). The 24 AVFs that remained patent at the end of the 4 years maintained a median blood flow rate > or =900 ml/min at all time points studied. Worth noting is that, five of them (20.8%) remained patent throughout the study with a blood flow rate consistently < or =500 ml/min. CONCLUSIONS: This study shows a very low rate of AVF thrombosis per patient-year at risk and a high actuarial survival of autogenous RC wrist AVFs, particularly of those having a blood flow rate >700 ml/min. Thus, a vascular access blood flow rate <700 ml/min appears to be a reliable cut-off point at which to start a closer monitoring of this parameter-which may lead to further investigations and possibly interventions relevant to the function of the AVFs.

Calcitriol pulse therapy and histology of parathyroid glands in hemodialysis patients.

BACKGROUND: Calcitriol pulse therapy (CPT) is considered the most appropriate treatment of secondary hyperparathyroidism (sHPTH). This treatment inhibits parathyroid hormone (PTH) synthesis and secretion, suppresses parathyroid cell proliferation and controls parathyroid gland growth. However, not much is known about the effect of such therapy on parathyroid morphology. METHODS: To investigate this, we studied all first parathyroidectomies (PTx, either total or subtotal) effected in 30 hemodialysis (HD) patients referred to our surgery department by five regional dialysis units in 2000-2001. Six patients were excluded from the study because of either the persistence or the precocious relapse (in the 1st 6 months post-operation) of sHPTH. Twenty-four HD patients were considered eligible as four parathyroid glands were ablated in each patient; 96 glands were then examined histologically. The cohort consisted of 16 males and 8 females with a mean age of 54 +/- 13 SD yrs (range 20-73) and a dialysis duration of 142 +/- 71 months (range 14-289). Data concerning calcitriol treatment (doses, administration route and treatment duration) were collected for each patient. The patients were subdivided into two groups according to the treatment effected in the months preceding PTx: group A (n=13), treated by either intravenous (i.v.) (n=12) or per os (n=1) CPT, and group B (n=11), not treated at all with calcitriol or vitamin D sterols. Parathyroid gland morphology and the parenchymal cell distribution of the parathyroid glands were evaluated by a semiquantitative assessment. Serum intact PTH (iPTH), alkaline phosphatase (AP), calcium (Ca) and phosphate (P) levels were studied pre- and post-PTx. RESULTS: Chief cells (CC) were found in all glands, either alone or associated with oxyphil cells (OC). OC were present in 13 of 24 patients (54%); however, it must be underlined that they were present 12 times in group A parathyroid glands (92%), and only once in group B (9%) (p<0.01). Nodular hyperplasia was found in 71% (17/24) of patients: 92% (12/13) in group A, and 45% (5/11) in group B (p<0.05). There were no significant differences in age, gender, dialysis duration, serum levels of iPTH, AP, Ca and P levels between the two groups. CONCLUSIONS: There was a strong association between OC presence in parathyroid glands and CPT. Furthermore, nodular hyperplasia appeared to be associated significantly with CPT. There is still speculation regarding the meaning of these CPT effects on parathyroid gland histology and consequently on sHPTH pathophysiology.