Quality of life as indicator of poor outcome in hemodialysis: relation with mortality in different age groups.

BACKGROUND: Physical, cognitive and psychosocial functioning are frequently impaired in dialysis patients and impairment in these domains relates to poor outcome. The aim of this analysis was to compare the prevalence of impairment as measured by the Kidney Disease Quality of Life- Short Form (KDQOL-SF) subscales between the different age categories and to assess whether the association of these subscales with mortality differs between younger and older dialysis patients. METHODS: This study included data from 714 prevalent hemodialysis patients, from 26 centres, who were enrolled in the CONvective TRAnsport STudy (CONTRAST NCT00205556, 09-12-2005). Baseline HRQOL domains were evaluated for patients <65 years, 65-74 years and over 75 years. Multivariable Cox proportional hazards analyses were performed to assess the relation between the separate domains and 2-year mortality. RESULTS: Emotional health was higher in patients over the age of 75 compared to younger patients (mean level 71, 73 and 77 for increasing age categories respectively, p = 0.02), whilst physical functioning was significantly lower in older patients (mean level 60, 48 and 40, p < 0.01). A low level of physical functioning (Hazard Ratio (HR) 1.72 [95%Confidence Interval (CI) 1.02-2.73]), emotional health (HR 1.85 [95% 1.30-2.63]), and social functioning (HR 1.59 [95% CI 1.12-2.26]), was individually associated with an increased 2-year mortality within the whole population. The absence of effect modification suggests no evidence for different relations within the older age groups. CONCLUSIONS: In dialysis patients, older age is associated with lower levels of physical functioning, whilst the level of emotional health is not associated with age. KDQOL-SF domains physical functioning, emotional health and social functioning are independently associated with mortality in prevalent younger and older hemodialysis patients.

Angiogenesis in peritoneal dialysis.

Long-term exposure to peritoneal dialysis fluid induces morphological alterations, including angiogenesis, leading to a loss of ultrafiltration (UF) capacity. We discuss the effect of different factors in peritoneal dialysis (PD) on angiogenesis. In addition, we describe the process of angiogenesis and the possible role of different cell types in the peritoneum upon PD contributing to new blood vessel formation. Furthermore, we review several interventions used in our rat PD exposure model to decrease angiogenesis in PD. Moreover, we show new data on the use of sunitinib to inhibit angiogenesis in this rat model. Although various interventions seem to be promising, well-randomised clinical trials showing absolute prevention of angiogenesis and UF failure are, yet, still missing. To make real progress in PD treatment, the aim should be to prevent angiogenesis as well as peritoneal fibrosis and PD-induced inflammation.

Immediate pain sensation is less with subcutaneous epoietin-beta compared to subcutaneous darbepoietin-alpha.

Although immediate pain sensation at the injection site is reported by patients, only limited data on comparison of pain at the injection site between erythropoiesis stimulating agents are available. Therefore, we compared the effect of subcutaneous epoietin-beta on immediate pain sensation to that of subcutaneous darbepoietin-alpha in a double blind, randomized controlled study. Adult patients, aged 18 - 75 years, treated with peritoneal dialysis or with stage 4 chronic kidney disease who in our unit are treated with subcutaneous darbepoietin-alpha for renal anemia for at least 3 months, were eligible for the study. After informed consent, patients received on one day four subcutaneous injections, two in each upper leg, in a fixed sequence, blinded to the patient and blinded to the investigator. Injections contained in a random order single dose epoietin-beta (0,3 ml = 4000 IU), darbepoietin-alpha (0,5 ml = 20 microg) and volume matched saline 0.9% placebo injections. Immediately after the four injections, whilst remaining sitting, the subject was requested to fill out one pain scale (Visual Analogue Scale (VAS)) and to verbally evaluate the pain experience (Verbal Pain Score (VPS)). Finally, the subject was requested to rank the four injections from least to most painful (Treatment Ranking). A total of 42 patients (22 male) participated in the study with a mean age of 56.8 +/- 1.9 years. The average VAS was lower for epoietin-beta (26.8 +/- 4.5 mm) compared to darbepoietin-alpha (58.1 +/- 4.6 mm; p < 0.01). Mean VAS for epoietin-beta did not differ from that of the two placebo saline solutions (0,3 ml 26.3 +/- 4.4 mm; 0,5 ml 18.4 +/- 3.2 mm). Mean VAS for darbepoietin-alpha was significantly higher than placebo (both p < 0.01). Similar observations were obtained for VPS (mean for epoietin-beta 1,3 +/- 0.2 and for darbepoietin-alpha 2.9 +/- 0.2; p < 0.01) and Treatment Ranking (mean for epoietin-beta 2.0 +/- 0.2 and for darbepoietin-alpha 3.2 +/- 0.2; p < 0.01). From the results it can be concluded that subcutaneous epoietin-beta caused statistically significant less pain sensation immediately after injection compared to subcutaneous darbepoietin-alpha . The pain caused by subcutaneous epoietin-beta injection was similar to that caused by placebo control injections whereas subcutaneous darbepoietin-alpha injection was significantly more painful than subcutaneous placebo injections.

Plasma adiponectin concentration has an inverse and a non linear association with estimated glomerular filtration rate in patients with K/DOQI 3 - 5 chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) is associated with an increased incidence of cardiovascular disease (CVD). A few studies have demonstrated elevated plasma adiponectin and leptin levels in CKD. The aims of this study were to assess whether 1) estimated glomerular filtration rate (eGFR) is associated with plasma leptin and adiponectin; and 2) adiponectin and leptin (partly) explain associations of CKD with endothelial dysfunction, insulin resistance, and low-grade inflammation in patients with K/DOQI Stage 3 - 5 CKD. METHODS: Baseline data from 91 patients with Stage 3 - 4 CKD in the anti-oxidant therapy in chronic renal insufficiency study, a randomized, double-blind, placebo-controlled trial, in which the effects of oxidative stress-lowering treatment on vascular function and structure were studied, and from 50 dialysis naïve patients, who took part in an open-label, randomized study that compared two peritoneal dialysis regimens, used in the analysis. All subjects for both the studies were recruited in the same centres. RESULTS: The association between eGFR and adiponectin was non-linear. In multivariate analysis, log-eGFR (unstandardized beta = 8.303 microg/ml, p < 0.0001) was the strongest determinant of adiponectin, and body mass index the strongest determinant of leptin (beta = 2.477 ng/ml, p < 0.0001). Plasma adiponectin and leptin did not modify the associations between eGFR and plasma von Willebrand factor or soluble vascular adhesion molecule-1. Plasma leptin had the strongest association with the homeostatic model assessment (HOMA-IR) index. Plasma C-reactive protein had no association with adiponectin or leptin. CONCLUSIONS: In patients with K/DOQI Stage 3 - 5 CKD, renal function had a significant non-linear inverse association with and was the strongest predictor of adiponectin. BMI was the strongest predictor of plasma leptin. Plasma adiponectin and leptin did not explain, and thus presumably are not involved in, the association between eGFR and some markers of endothelial dysfunction.

Nephrectomy elicits impact of age and BMI on renal hemodynamics: lower postdonation reserve capacity in older or overweight kidney donors.

Renal functional reserve could be relevant for the maintenance of renal function after kidney donation. Low-dose dopamine induces renal vasodilation with a rise in glomerular filtration rate (GFR) in healthy subjects and is thought to be a reflection of reserve capacity (RC). Older age and higher body mass index (BMI) may be associated with reduced RC. We therefore investigated RC in 178 consecutive living kidney donors (39% males, age 48 +/- 11 years, BMI 25.5 +/- 4.1). RC was determined as the rise in GFR ((125)I-iothalamate), 4 months before and 2 months after donor nephrectomy. Before donor nephrectomy, GFR was 114 +/- 20 mL/min, with a reduction to 72 +/- 12 mL/min after donor nephrectomy. The dopamine-induced rise in GFR of 11 +/- 10% was reduced to 5 +/- 7% after donor nephrectomy (p < 0.001). Before donor nephrectomy, older age and higher BMI did not affect reserve capacity. After donor nephrectomy, the response of GFR to dopamine independently and negatively correlated with older age and higher BMI. Moreover, postdonation reserve capacity was absent in obese donors. The presence of overweight had more impact on loss of RC in younger donors. In conclusion, donor nephrectomy unmasked an age- and overweight-induced loss of reserve capacity. Younger donors with obesity should be carefully monitored.

Preglomerular and postglomerular basal diameter changes and reactivity to angiotensin II in obese rats.

AIM AND METHODS: Obesity in humans is associated with proteinuria and an increased glomerular filtration, possibly related to an increase in glomerular capillary pressure. We investigated in obese and lean Zucker rats (10-12 weeks old) whether this might be related to alterations in the diameter of preglomerular and postglomerular microvessels and their reactivity to the resistance regulator angiotensin II (AngII), using the hydronephrotic kidney model. RESULTS: The obese rats exhibited a hyperinsulinaemic, euglycaemic state and hypertension. Urinary protein concentration and fluid intake were both increased threefold. Basal diameters of distal interlobular arteries (ILAs) and afferent arterioles (AAs) were larger in the obese rat than in the lean rat (ILA: 25.7 +/- 0.3 vs. 23.0 +/- 0.4 microm and AA: 18.8 +/- 0.3 vs. 16.7 +/- 0.5 microm, respectively; p

Subjective sleep efficiency of hemodialysis patients.

BACKGROUND: Sleep disturbances have a major influence on quality of life. A commonly used measure of sleep disturbances is sleep efficiency. The purpose of this study was to investigate the prevalence of decreased subjective sleep efficiency in hemodialysis patients. An additional goal was to identify clinical, dialysis or laboratory parameters that are independently associated with decreased sleep efficiency. METHODS: Adult stable hemodialysis patients (n = 112) filled out a sleep questionnaire during a three day investigation period. In addition, healthy control subjects (n = 44) filled out the same questionnaire. From this questionnaire sleep efficiency (ratio of total sleep time to time spent in bed) was derived as a measure for sleep disturbances in this population. Laboratory, demographic and dialysis data were collected during the investigation period. For statistical analysis linear regression models were used. RESULTS: Median subjective sleep efficiency in hemodialysis patients was 80%, which was significantly less compared to the median subjective sleep efficiency of control subjects of 88% (p pound 0.05). Approximately 40% of the patients used sleep medication. However, less than 20% of them indicated improved sleep behavior when using these drugs. Elevated levels of phosphate and urea correlated independently with impaired sleep efficiency. Hemoglobin levels between 10 and 12 g/dl were associated with better sleep efficiency. CONCLUSION: In conclusion, decreased sleep efficiency was frequently reported in hemodialysis patients and can be associated with biochemical parameters. Hemoglobin, phosphate and urea levels can affect subjective sleep efficiency.

Mild-to-moderate renal impairment is associated with platelet activation: a cross-sectional study.

The high incidence of cardiovascular disease in patients with moderate renal impairment is not fully explained by traditional atherothrombotic risk factors. Independently from these factors, blood platelet activation may increase the cardiovascular disease risk of patients with mild-to-moderate renal impairment. Blood platelet activation has not been studied in nondiabetic patients with mild-to-moderate renal impairment. Therefore, we measured the extent of platelet activation by means of fluorescence cytometry in 93 nondiabetic patients with MDRD-estimated creatinine clearance ranging from 13 - 63 ml/min/1.73 m2. As platelet activation parameters we used the expression of CD62P (P-selectin), CD 63 (glycoprotein 53), PAC-1 (activated fibrinogen receptor), CD42b (von Willebrand factor receptor) and CD41 (fibrinogen receptor) on the platelet surface membrane. The expression of CD62p, CD63 and PAC-1 was statistically significantly inversely related to the estimated glomerular filtration rate in these patients (standardized b -0.28, -0.32 and -0.39, respectively). We conclude that nondiabetic mild-to-moderate renal impairment is associated with blood platelet activation. Whether this contributes to the increased cardiovascular risk in these patients needs further study.

Differences in peritoneal response after exposure to low-GDP bicarbonate/lactate-buffered dialysis solution compared to conventional dialysis solution in a uremic mouse model.

BACKGROUND: Long-term exposure of conventional peritoneal dialysis (PD) fluid is associated with structural membrane alterations and technique failure. Previously, it has been shown that infiltrating IL-17-secreting CD4+T cells and pro-fibrotic M2 macrophages play a critical role in the PD-induced pathogenesis. Although more biocompatible PD solutions are recognized to better preserve the peritoneal membrane integrity, the impact of these fluids on the composition of the peritoneal cell infiltrate is unknown. MATERIALS AND METHODS: In a uremic PD mouse model, we compared the effects of daily instillation of standard lactate (LS) or bicarbonate/lactate-buffered solutions (BLS) and respective controls on peritoneal fibrosis, vascularisation, and inflammation. RESULTS: Daily exposure of LS fluid during a period of 8 weeks resulted in a peritoneal increase of αSMA and collagen accompanied with new vessel formation compared to the BLS group. Effluent from LS-treated mouse showed a higher percentage of CD4+ IL-17+ cell population while BLS exposure resulted in an increased macrophage population. Significantly enhanced inflammatory cytokines such as TGFß1, TNFα, INFγ, and MIP-1ß were detected in the effluent of BLS-exposed mice when compared to other groups. Further, immunohistochemistry of macrophage subset infiltrates in the BLS group confirmed a higher ratio of pro-inflammatory M1 macrophages over the pro-fibrotic M2 subset compared to LS. CONCLUSION: Development of the peritoneal fibrosis and angiogenesis was prevented in the BLS-exposed mice, which may underlie its improved biocompatibility. Peritoneal recruitment of M1 macrophages and lower number of CD4+ IL-17+ cells might explain the peritoneal integrity preservation observed in BLS-exposed mouse.

Acute effects of hemodialysis on salivary flow rate and composition.

AIMS: To evaluate acute effects of hemodialysis (HD) on the salivary flow rate, pH and biochemical composition before, during and after completion of a dialysis session. MATERIAL AND METHODS: Unstimulated whole saliva (UWS) and chewing-stimulated whole saliva (CH-SWS) were collected in 94 HD patients. Salivary flow rate, pH, concentrations of total protein, albumin, cystatin C, secretory immunoglobulin A (S-IgA) and of sodium, potassium and urea were measured. RESULTS: HD had an acute stimulating effect on the salivary flow rate (UWSbefore = 0.30+/-0.22 ml/min, UWSduring = 0.39+/-0.25 ml/min, p < 0.005). The mean pH of UWS showed a small but significant increase during HD mainly due to an increased watery secretion from the salivary glands. The salivary biochemical constituents changed markedly, but no significant difference in output was found. The electrolyte concentration did not change significantly during dialysis. The level of urea in CH-SWS declined to 40% (Ureabefore = 25.+/-6.4 mmol/l, Ureaduring = 15.3+/-4.5 mmol/1). CONCLUSIONS: This study shows that HD has significant acute effects on both salivary secretion rate and protein concentrations in saliva. We conclude that the observed changes in salivary concentrations and proteins are mainly due to an increased watery secretion from the salivary glands.

Sino-nasal bony and cartilaginous destruction associated with cocaine abuse, S. aureus and antineutrophil cytoplasmic antibodies.

Three male patients aged 29, 30 and 34 years and a 36-year-old female are reported with nasal septum perforation and a history of cocaine abuse. Two of the patients also had a perforation of the hard palate. In all four, antineutrophil cytoplasmic antibodies (ANCA) were found. One had a cytoplasmic immunofluorescence-staining pattern (c-ANCA), the other three showed a perinuclear staining pattern (p-ANCA). Furthermore, all patients were found to be nasal carriers of S. aureus. We hypothesise that tissue damage to the nasal and palatal area in patients using cocaine may partly be mediated by the presence of ANCA antibodies. Furthermore, we speculate that S. aureus facilitates the development of these ANCA antibodies.

[New study evaluating online haemodiafiltration for the reduction of cardiovascular morbidity and mortality in patients undergoing chronic haemodialysis]. / Nieuw onderzoek naar online-hemodiafiltratie voor de vermindering van cardiovasculaire morbiditeit en mortaliteit bij patiënten die chronisch worden behandeld met hemodialyse.

Removal of uraemic toxins can be increased by online haemodiafiltration. At present, it is unclear whether online haemodia-filtration ultimately improves clinical outcomes in chronic haemodialysis patients. The Dutch 'Convective transport study' (CONTRAST) is an ongoing trial comparing standard haemodialysis with online haemodiafiltration. This randomised controlled trial will provide substantial clinical evidence on the effects of haemodiafiltration on fatal and non-fatal cardiovascular events and all-cause mortality, compared with standard haemodialysis.

Risk factors determining active urinary stone formation in patients with urolithiasis.

AIMS: The goal of clinical and metabolic evaluation of patients with urinary stones is to identify patients at high risk for recurrent stone formation and as such, to allow the practitioner to suggest preventive therapies. However, knowledge about risk factors for active stone formation in patients with urolithiasis is limited. This study was initiated to assess the significance of several metabolic and clinical parameters for the determination of the risk of active stone formation. METHODS: Study in 320 consecutive outpatients referred to our clinic for metabolic analysis. Clinical and metabolic parameters were determined by standardized procedures of questionnaires, serum biochemical profiles and urinalysis. RESULTS: In 21.5% of 284 patients with complete data stone formation was active. Hypercalciuria, hypocitraturia and urinary tract infections had odds ratios for active stone formation above 2.5, whereas the odds ratio of a positive family history was 0.38. Hyperuricosuria, hyperoxaluria and a low urinary volume did not influence the risk for active stone formation. CONCLUSION: The risk profile for active stone formation differs from the risk profile for urolithiasis in general. Metabolic evaluation and determination of those risk factors in patients with urolithiasis might improve the estimation of the risk of future stone formation.

Angiotensin-converting enzyme inhibitors and progression of nondiabetic chronic renal disease.

In recent years, considerable attention has focused on the possibility that some classes of antihypertensive agents may confer a greater renoprotective effect in retarding the progression of chronic renal insufficiency. Experimental studies in rats have demonstrated that the sustained increase in glomerular capillary pressure evoked in response to loss of renal mass produces a destructive sclerosing reaction. Administration of angiotensin-converting enzyme inhibitors decreases glomerular capillary pressure with a resultant reduction of glomerular sclerosis, suggesting that angiotensin-converting enzyme inhibitor therapy may protect the injured kidney from hemodynamically mediated glomerular damage. On the basis of these experimental observations, many studies have attempted to investigate whether angiotensin-converting enzyme inhibitors can slow the progression of chronic renal disease in humans. We surveyed the literature critically and concluded that, the data from animals notwithstanding, the majority of studies in humans have been nonrandomized, of too short duration, or confounded by investigative difficulties. Therefore, we cannot yet conclude that angiotensin-converting enzyme inhibitors modify the rate at which renal disease progresses in nondiabetic patients.

Effects of calcium antagonists on renal hemodynamics and progression of nondiabetic chronic renal disease.

In recent years, substantial investigative attention has focused on therapeutic regimens that could retard the progression of chronic renal insufficiency. Emphasis has been placed on the effects of antihypertensive treatment on renal hemodynamics and preservation of renal function. It has been suggested that some classes of antihypertensive agents may confer a greater renoprotective effect, especially agents that lower glomerular capillary pressure. Conversely, by virtue of their ability to preferentially dilate the afferent arteriole calcium antagonists theoretically could favor an increase in glomerular capillary pressure thereby accelerating the decline of renal function. In this review we survey the literature critically and conclude that in patients with essential hypertension and in patients with chronic renal insufficiency, calcium antagonists effectively reduce systemic blood pressure while maintaining glomerular filtration rate and effective renal plasma flow. Preliminary results from a few long-term studies suggest that calcium antagonists may even attenuate the decline in renal function of patients with chronic renal failure. The majority of studies in humans, however, have been nonrandomized, of too short duration, or confounded by investigative difficulties precluding definite conclusions whether calcium antagonists have renoprotective effects. Although the possibility that calcium antagonists may retard progression of renal disease remains to be ascertained, the available evidence indicates that calcium antagonists may be used in patients with renal functional impairment without further exacerbating renal function.

Capillary recruitment is impaired in essential hypertension and relates to insulin's metabolic and vascular actions.

OBJECTIVE: In patients with essential hypertension, defects in both the metabolic and vascular actions of insulin have been described. Impaired microvascular function, a well-established abnormality in essential hypertension, may explain part of these defects. In the present study we investigated whether microvascular function is impaired in essential hypertension and relates to insulin's metabolic and vasodilatatory actions. METHODS: We measured 24-h ambulatory blood pressure, capillary recruitment after arterial occlusion, and skin blood flow responses to iontophoresis of acetylcholine and sodium nitroprusside in 18 subjects with untreated essential hypertension and in 18 control subjects. Whole body insulin sensitivity and leg insulin-mediated vasodilatation were assessed with the hyperinsulinaemic clamp technique and plethysmography. RESULTS: Hypertensive, as compared to normotensive, subjects had a decreased insulin sensitivity (0.8+/-0.3 vs. 1.7+/-0. 6 mgkg(-1)min(-1) per pmoll(-1); P<0.001), capillary recruitment after arterial occlusion (21.5+/-5.8 vs. 45.9+/-10.4%; P<0.001), acetylcholine-mediated vasodilatation (331+/-84 vs. 688+/-192%; P<0. 001), and insulin-mediated vasodilatation (median 29.3 vs. 47.2%; P<0.05). Correlation analyses with adjustment for sex, age, body mass index and waist-to-hip ratio showed significant relationships of capillary recruitment after arterial occlusion with blood pressure (r=-0.68; P<0.01), insulin sensitivity (r=+0.55; P<0.01) and insulin-mediated vasodilatation (r=+0.51; P<0.05), which extended from the normotensive to the hypertensive range. CONCLUSION: Skin microvascular function is associated with blood pressure and insulin's metabolic and vasodilatatory actions, both in normotensive and hypertensive subjects. These findings offer a potential mechanistic explanation of the links among insulin resistance, impaired insulin-mediated vasodilatation and hypertension.

Hepcidin in chronic kidney disease: not an anaemia management tool, but promising as a cardiovascular biomarker.

Hepcidin is a key regulator of iron homeostasis and plays a role in the pathogenesis of anaemia of chronic disease. Its levels are increased in patients with chronic kidney disease (CKD) due to diminished renal clearance and an inflammatory state. Increased hepcidin levels in CKD patients are supposed to be responsible for functional iron deficiency in these patients and contribute to renal anaemia and resistance to erythropoiesis-stimulating agents. Therefore, hepcidin was purported to be useful as a management tool guiding treatment of renal anaemia. Furthermore, since hepcidin is associated with iron accumulation in macrophages in the vessel wall inducing oxidative stress and atherosclerosis, it has been speculated that hepcidin might function as a biomarker of cardiovascular disease. In this descriptive review, the merits of hepcidin with respect to its role in the pathophysiology of renal anaemia in CKD patients, its presumptive role as a practical diagnostic tool guiding management of renal anaemia, and its possible usefulness as a prognostic biomarker will be discussed.

Birth weight relates to blood pressure and microvascular function in normal subjects.

OBJECTIVE: The relationship between low birth weight and elevated blood pressure in adult life is well established but presently unexplained. Both microvascular dysfunction and insulin resistance have been proposed as a possible explanation. We have examined the relation between birth weight and blood pressure in 30 healthy subjects exhibiting a wide range of insulin sensitivity, and assessed whether microvascular function and/or insulin resistance may underlie this relationship. METHODS: Birth weight data were obtained from birth announcements. Blood pressure was measured with an ambulatory blood pressure monitor and insulin sensitivity was assessed by the hyperinsulinaemic, euglycaemic clamp technique. Microvascular function, i.e. capillary recruitment and endothelium-dependent and -independent vasodilatation in the skin, was evaluated by videomicroscopy and iontophoresis of acetylcholine and sodium nitroprusside. RESULTS: Birth weight was significantly associated with blood pressure (r= -0.50; P< 0.05), capillary recruitment (r= +0.52; P< 0.05), acetylcholine-mediated vasodilatation (r= +0.40; P< 0.05), insulin sensitivity (r= +0.62; P< 0.01) and waist-to-hip ratio (r= -0.42; P< 0.05). Regression analysis showed a significant association of birth weight with 24 h systolic blood pressure (regression coefficient: -7.6 mmHg/kg; 95% confidence interval: -13.0 to -1.0). Adjustment for capillary recruitment and waist-to-hip ratio decreased the regression coefficient by 39 and 41%, respectively. The results were similar after adjustment for age, sex or body mass index. CONCLUSION: These results suggest that capillary recruitment and body fat distribution may partly explain the relationship between birth weight and blood pressure.

A scanning electron microscopy analysis of a spontaneous hemodialysis catheter fracture.

Central venous catheters have become increasingly important in hemodialysis treatment. With their increased use, catheter-related problems will be seen more frequently, and more rare complications may be observed. We describe the first case of asymptomatic spontaneous breakdown of a tunneled cuffed silicone catheter used for long-term hemodialysis treatment. This was discovered on removal of the catheter, leaving behind a catheter fragment in the left lower pulmonary lobe. An extensive scanning electron microscopy study showed accumulation of lumps of nonsilicone material at the place of the fracture, leading to severe disruption of the original cross-linked elastomer structure. Using energy-dispersive X-ray spectral analysis, which shows all elements with an atomic number of 11 or greater in a material, we found the lumps were aggregates of barium sulfate particles used to visualize the catheter on fluoroscopy. We suggest that the use of too small or too many barium sulfate particles led to high viscosity of the raw silicone before polymerization, causing improper mixing of barium sulfate particles in the silicone matrix. This resulted in insufficient removal of admixed air bubbles and unequal dispersion of barium sulfate, with the potential for weak spots after extrusion of the silicone into its definitive shape. With the increasing use of hemodialysis catheters for prolonged periods, catheter-related complications related to materials or manufacturing errors can be expected to occur more often.

Renal effects of intravenous amino acid administration in humans with and without renal disease: hormonal correlates.

In the early 1980s, renewed interest was focused on the possible protective effect of protein-restricted diets on the progression of human renal insufficiency. This resulted from observations in several models of experimental renal failure in which protein-restricted diets attenuated the progression of renal insufficiency. Micropuncture studies in subtotally nephrectomized rats and rats with other causes of renal insufficiency had shown that glomerular hyperfiltration occurred in remnant glomeruli to compensate for the loss of renal function. However, such rats developed progressive glomerular sclerosis. In rats fed a protein-restricted diet, such glomerular hyperfiltration did not occur and the development of renal insufficiency was postponed. Thus, it was hypothesized that the compensatory hyperfiltration of remnant glomeruli was ultimately harmful to the kidneys. At the same time, concomitant research was started to establish methods to show the presence of glomerular hyperfiltration in humans, in an attempt to trace patients who could benefit from protein-restricted diets. Thus, the effects of an acute protein load, given as a meat meal or intravenous administration of amino acids, on renal hemodynamics were investigated resulting in the introduction of the concept of renal reserve capacity. In the present report, the effects of intravenously administered amino acids on renal hemodynamics of subjects with and without renal disease will be discussed. Special interest will be focused on the amino acid-induced hormonal changes and their involvement in the renal hemodynamic changes observed during amino acid infusion.