Daily weight gain and protein catabolic rate are lower over the long interdialytic interval

BACKGROUND: The interdialytic weight gain (IDWG) and protein catabolic rate (PCR), expressed per 24 hours (daily), are usually assumed to be stable over the week in chronic hemodialysis (HD) patients. METHODS: We studied different HD patient groups at different time points (study 1 in 1993: n = 48, study 2 in 1999: n = 16, study 3 in 2000: n = 112). Daily IDWG (calculated from post- and pre-dialysis body weight and interdialytic interval) and nPCR (calculated from kinetic modeling) were compared over short (2 days) and long (3 days) intervals. RESULTS: In all groups of HD patients studied, both daily IDWG and nPCR were significantly (p < 0.05) lower (IDWG by 7-15%, nPCR by 5-6%) over long than short interdialytic intervals. This difference was observed whether or not blood sampling was planned after the long interval. This suggests selfrestriction of dietary intake over the long interdialytic interval. CONCLUSIONS: Daily IDWG and nPCR are lower over the long interdialytic interval. Studies should thus define or even standardize the period of time over which IDWG and nPCR are calculated.     

Pathological aspects of beta(2)-microglobulin amyloidosis

Histology remains the gold standard to diagnose beta(2)-microglobulin amyloidosis (A beta(2)M). Two diagnostic criteria are required: positive Congo red staining with typical birefringence under polarized light and immunostaining of amyloid deposits with a labeled anti-beta(2)M antibody. A beta(2)M is preferentially located in the joints. Small deposits are also found in various organs, mainly the heart and gastrointestinal tract. Pathologic studies have demonstrated a high prevalence of articular A beta(2)M early in the course of hemodialysis and peritoneal dialysis, antedating clinical manifestations by several years. The stages of beta(2)M amyloid formation have been delineated: beta(2)M amyloid deposits first on the surface of the cartilage, in the absence of macrophages (stage 1), and subsequently involves capsules and synovia (stage 2), with eventual recruitment of macrophages around large beta(2)M amyloid deposits (stage 3). Clinical manifestations are likely associated with the inflammation observed in stage 3. The factors triggering the fibrillar precipitation of beta(2)M remain unknown. Macrophages do not play a role: their presence is the consequence rather than the cause of beta(2)M amyloid deposits. Several substances coprecipitated with beta(2)M amyloid have been incriminated: highly sulfated glycosaminoglycans such as chondroitin or keratan sulfate, antiproteases such as alpha(2)-macroglobulin, and apolipoprotein E. As yet, no definitive conclusion has been reached.     

Progression rate of Chinese herb nephropathy: impact of Aristolochia fangchi ingested dose

Sir, Muniz Martinez et al. [1] report, in 71 patients with Chineseherbs nephropathy (CHN), an interesting relationship betweenthe total amount of ingested Stephania tetrandra/Aristolochiafangchi herbs and the progression rate of renal failure. Fiveyears ago we reached a similar conclusion in an analysis of15 patients: we demonstrated a striking relationship betweenthe duration of Chinese herbs     

Thrombotic microangiopathy induced by long-term interferon-β therapy for multiple sclerosis: a case report

We report the case of a 53-year-old woman treated for 8 years with Betaferon? (interferon-β-1b), who developed mild renal failure with hypertension, proteinuria and glomerular hematuria. Kidney biopsy was consistent with thrombotic microangiopathy (TMA). Considering the strong evidence of interferon-α causing TMA and the numerous immunomodulatory activities shared by INF-α and -β, we incriminated Betaferon as the etiological agent of TMA in our patient. To our knowledge, it is the first time such an association has been published.     

Serum Fetuin-A Levels Are Associated with Vascular Calcifications and Predict Cardiovascular Events in Renal Transplant Recipients

Summary

Background and objectives

Vascular calcifications predict cardiovascular disease, the major cause of death in renal transplant recipients (RTRs). We studied the determinants of fetuin-A, a potent circulating calcification inhibitor encoded by the AHSG gene, and tested its association with vascular calcifications and long-term survival and cardiovascular events (CVEs) in RTRs.

Design, setting, participants, & measurements

Two hundred seventy-seven prevalent RTRs from a single center were included. CVEs and deaths were prospectively recorded during a 5-year follow-up.

Results

Independent determinants of lower serum fetuin-A levels were lower plasma cholesterol, the AHSG rs4918 G allele, and history of smoking. Low serum fetuin-A level was a determinant of aortic calcifications (assessed using spiral CT). Low fetuin-A levels (≤0.47 g/L, first quintile) were independently associated with CVEs and deaths (hazard ratio = 1.83; 95% confidence interval, 1.07 to 3.04). The association was confirmed for all-cause mortality, and the major adverse cardiovascular endpoints were analyzed separately. Patients with low fetuin-A and high high-sensitivity C-reactive protein (>4.36 mg/L, fourth quintile) levels had a 3.5-fold increased risk of all-cause mortality and CVEs. In the presence of inflammation, CVE-free survival was influenced by common variants in the AHSG gene.

Conclusions

These data show that low fetuin-A levels are independently associated with aortic calcifications and a higher risk of CVEs and mortality. They support fetuin-A as a circulating biomarker able to identify RTRs at risk for vascular calcifications and CVEs.     

X-ray Scattering Analysis of Human Stratum Corneum Treated by High Voltage Pulses

Pharmaceutical Research -     

Mineralocorticoids in the management of primary adrenocortical insufficiency

Plasma renin activity (PRA) and plasma volume (PV) were determined in 22 adult patients treated for Addison's disease (AD) and reporting at the clinic for follow-up. Mean PRA was thrice the upper limit of normal (9.1 +/- 7.1 ng/ml/h (SD)) and mean PV was decreased (87% +/- 11 (SD)), consistent with residual hypovolemia in most patients, despite conventional treatment with both fluorocortisol (FF) and cortisone acetate. There was an inverse relationship between PRA and PV. Both PRA and PV were significantly correlated with FF dosage. On the other hand, no correlation was found between PV and either systolic or diastolic blood pressure (BP), while PRA was significantly correlated with systolic but not diastolic BP. Four patients were persistently hypertensive (diastolic BP greater than 100 mmHg) with elevated PRA in 3, associated with a definitely low PV in two cases. Two of these patients were progressively taken off FF, so as to control BP. Thus, in view of the not infrequent occurrence of arterial hypertension in AD patient on conventional treatment, we would warn against attempts at normalizing PV and PRA by means of FF, irrespective of BP in asymptomatic cases. In fact, when hypertension develops, reduction or sometimes withdrawal of FF may be recommended as a first therapeutic step.