Fenofibrate is a potent hypolipemic agent, widely used in patients with renal insufficiency in whom dyslipidemia is frequent. A moderate reversible increase in creatinine plasma levels is an established side effect of fenofibrate therapy, which mechanism remains unknown. We have previously reported that in 13 patients with normal renal function or moderate renal insufficiency, two weeks of fenofibrate therapy increased creatininemia without any changes in renal plasma flow and glomerular filtration rate [1]. In 13 additional patients, muscular enzymes (AST, GPT, CPK, LDH) and myoglobin were measured before and after 2 weeks on fenofibrate, and the values of creatininemia obtained by the Jaffé technique and HPLC were compared. CPK and AST activity and plasma myoglobin increased in 2 patients with fenofibrate, but muscular enzymes remained unchanged in the population as a whole, and were not correlated to the changes in creatininemia. The changes in creatininemia induced by fenofibrate measured by the Jaffé technique were strongly correlated to those measured by HPLC (r² = 0.675, p = 0.0006). Analysis of the pooled data of the two arms of the study showed in 26 patients that two weeks of fenofibrate therapy efficiently reduced total cholesterol and triglycerides plasma levels, and raised creatininemia from 139 ± 8 to 160 ± 10 µmol/l (p < 0.0001), but confirmed that creatininuria also increased to the extent that creatinine clearance remained unchanged (68 ± 6 vs. 67 ± 6 ml/min, n.s.). It is concluded that the increase in creatininemia induced by fenofibrate in renal patients does not reflect an impairment of renal function, nor an alteration of tubular creatinine secretion, and is not falsely increased by a dosage interference. Fenofibrate-induced increase of daily creatinine production is neither readily explained by accelerated muscular cell lysis. It is proposed that fenofibrate increases the metabolic production rate of creatinine.

The aim of this study was to estimate the incidence of COVID-19 disease in the French national population of dialysis patients, their course of illness and to identify the risk factors associated with mortality. Our study included all patients on dialysis recorded in the French REIN Registry in April 2020. Clinical characteristics at last follow-up and the evolution of COVID-19 illness severity over time were recorded for diagnosed cases (either suspicious clinical symptoms, characteristic signs on the chest scan or a positive reverse transcription polymerase chain reaction) for SARS-CoV-2. A total of 1,621 infected patients were reported on the REIN registry from March 16th, 2020 to May 4th, 2020. Of these, 344 died. The prevalence of COVID-19 patients varied from less than 1% to 10% between regions. The probability of being a case was higher in males, patients with diabetes, those in need of assistance for transfer or treated at a self-care unit. Dialysis at home was associated with a lower probability of being infected as was being a smoker, a former smoker, having an active malignancy, or peripheral vascular disease. Mortality in diagnosed cases (21%) was associated with the same causes as in the general population. Higher age, hypoalbuminemia and the presence of an ischemic heart disease were statistically independently associated with a higher risk of death. Being treated at a selfcare unit was associated with a lower risk. Thus, our study showed a relatively low frequency of COVID-19 among dialysis patients contrary to what might have been assumed.

Introduction and aims: Vascular calcification is common in patients suffering from advanced chronic kidney disease (CKD), yet little is known about vascular calcification and arterial stiffness in the early stages of renal dysfunction. We evaluated, in patients suffering from CKD 3, the arterial vascular damage by means of the measurement of arterial stiffness and the coronary calcium score. Methods: Eleven patients (7 M, 4 f, aged 64±7 years) with mild to moderate renal failure were enrolled. We deliberately excluded patients with diabetes and previous history of heart disease from this study; we did this in order to exclude the interference of other pathologies apart from functional kidney insufficiency in the genesis of vascular alterations. the causes of renal failure were nephroangiosclerosis (73%), membranous glomerulonephritis (18%), and interstitial nephritis (9%). all the patients underwent the assessment of coronary calcification by means of multi-detector Ct (expressed as calcium score [Cs] according to agatston score), arterial stiffness by pulse wave velocity (pWV) measurement, common carotid intima-media thickness (iMt) by B-mode Us scan, and left ventricular mass index by echocardiography. renal function (Gfr) was evaluated using the Cockroft and Gault formula. Blood samples were drawn for the measurement of serum creatinine, lipid profile, glycidic profile, electrolytes, hOMa index, etc. Results: the main results are summarized in the table. Whilst the calcium score (Cs) was abnormal in only one patient (the remaining patients had a Cs <50 hU), the pWV and iMt were high in all of them. No substantial alterations in the lipid profile and hOMa index were present. Conclusions: Our data, albeit obtained in a small number of patients, show that in the early stages of chronic renal failure, in the absence of diabetes and cardiac involvement, vascular calcification is only rarely present. On the contrary, arterial stiffening, as shown by pWV and iMt, starts very early, even in the presence of a normal lipid profile and insulin resistance. further studies in larger groups are needed to confirm this results, as well as to understand at which moment or which factors lead to the development of the extensive vascular calci-fication observable in the advanced stages of CKD. Table. Results Variable Mean±SD GFR, mL/min 40.6±10 Total cholesterol, mg/dL 198±35 LDL cholesterol, mg/dL 111±29 HDL cholesterol, mg/dL 53±16 Triglycerides, mg/dL 183±93 HOMA index, % 1.9±1.5 PWV, m/sec 10.5±1.6 ccIMT, mm 0.8± 1.2 LVM index, g/m 2 110±41 CS (HU)* 0-1074 *Expressed as range. increased pulse wave velocity (pWV), a marker of arterial stiffness, is considered a strong predictor of cardiovascular mortality both in general and in the renal-disease population. however, it is unknown whether it may be affected by the rapid variations in the fluid status induced by treatment in dialysis (hD) patients. We studied 13 patients (6 M, 7 f, 65±12 years) on thrice-weekly chronic hD treatment in a study session after the longest interdial...

To elucidate the pathophysiology of dietary calcium independent hypercalciuria, 42 calcium stone formers (Ca SF) were selected because they had on free diet a calciuria greater than 0.1 mmol/kg/day. For four days they were put on a diet restricted in calcium (Ca RD) by exclusion of the dairy products. They collected 24 hour urines on free diet and on day 4 of Ca RD as well as the two-hour fasting urines on the morning of the day 5 and the four-hour urines passed after an oral calcium load of 1 g, for measurement of creatinine, Ca, PO4, urea and total hydroxyprolinuria (THP). On day 5 fasting plasma concentrations of Ca, PO4, intact PTH, Gla protein, calcidiol and calcitriol were measured. The patients were firstly classified into dietary hypercalciuria (DH, 18 patients) and dietary calcium-independent hypercalciuria (IH, 24 patients) on the basis of the disappearance or not of hypercalciuria on Ca RD. Then the patients with IH were subclassified into absorptive hypercalciuria (AH) because of normal fasting calciuria (8 patients) and into fasting hypercalciuria (16 patients). Fasting hypercalciuric patients were subsequently divided according to the PTH levels into renal hypercalciuria (RH, 1 patient) with elevated fasting PTH becoming normal after the Ca load and undetermined hypercalciuria (UH, 15 patients) with normal PTH levels. Furthermore, their vertebral mineral density (VMD) was measured by quantitative computerized tomography which was normal in DH (91 +/- 6% of the normal mean for age and sex) but was decreased in IH to 69 +/- 4%. No difference in VMD was observed between AH and UH. Urinary excretions of urea, phosphate and THP was higher in IH than in DH and comparable in AH and UH. Sodium excretion Ca RD was the same in all groups and subgroups as well as the plasma parameters. Plasma calcitriol was increased in IH and DH comparatively to normal in spite of normal plasma calcidiol. Calciuria increase after oral calcium load, an index of Ca absorption, was higher in IH than in controls and comparable in IH and DH as well as in the three subgroups of IH. From these data and correlation studies in IH it is concluded: (1.) VMD is decreased in Ca stone formers with IH but not in those with DH, making the distinction of these two groups of hypercalciuria patients clinically relevant.(ABSTRACT TRUNCATED AT 400 WORDS)

In hypertensive patients with chronic renal failure enalapril slows progression towards end stage renal failure compared with beta blockers. This effect was probably not mediated through controlling blood pressure.

Given comparable control of plasma calcium, phosphate and 25-OH vitamin D, PTH control is comparable in both strategies. Sevelamer does not induce greater vitamin D depletion than CaCO(3). The transient decrease of serum bicarbonate after discontinuation of CaCO(3) in the sevelamer group suggests a less optimal prevention of acidosis. The sevelamer-induced decrease in LDL cholesterol gives this drug a potential advantage in cardiovascular prevention.

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This study suggests a bone-sparing effect of serum leptin in haemodialysis patients only when the serum levels of leptin were higher than the presumed threshold of blood-brain transport saturation. Higher leptin levels in post-menopausal female haemodialysis patients than in male patients may account for their slower bone loss with ageing.