Refeeding Syndrome in Historical Perspective:Its First Description by Rodulfus Glaber (1033)

The refeeding syndrome refers to a potentially fatal situation hallmarked by sudden death and cardiac decompensation that can occur when amalnourished person is refeeded. Electrolyte disturbances are currently considered to play a role in its pathophysiology. In the absence of laboratorymeasurements, clinical descriptions of the refeeding syndrome so far date back to the early post world war II period, including anecdotal evidencefrom victims of the nazi concentration camps. Here we want to draw attention to a medieval description that fulfils the clinical description of therefeeding syndrome by the French monk, Rodolfus Glaber. He writes about people suffering from the Burgundy famine (1033) that “even when theyreceived food, they became distended and died immediately” (fourth book, chapter 4, 13). With this reference to medieval famine, we wish to paytribute to those who suffered from the holocaust 75 years after their liberation

Vitamin D and Calcium Supplementation Accelerates Randall's Plaque Formation in a Murine Model

Most kidney stones are made of calcium oxalate crystals. Randall\u27s plaque, an apatite deposit at the tip of the renal papilla, is considered to at the origin of these stones. Hypercalciuria may promote Randall\u27s plaque formation and growth. We analyzed whether long-term exposure of Abcc6 mice (a murine model of Randall\u27s plaque) to vitamin D supplementation, with or without a calcium-rich diet, would accelerate the formation of Randall\u27s plaque. Eight groups of mice (including Abcc6 and wild type) received vitamin D alone (100,000 UI/kg every 2 weeks), a calcium-enriched diet alone (calcium gluconate 2 g/L in drinking water), both vitamin D supplementation and a calcium-rich diet, or a standard diet (controls) for 6 months. Kidney calcifications were assessed by 3-dimensional microcomputed tomography, μ-Fourier transform infrared spectroscopy, field emission-scanning electron microscopy, transmission electron microscopy, and Yasue staining. At 6 months, Abcc6 mice exposed to vitamin D and calcium supplementation developed massive Randall\u27s plaque when compared with control Abcc6 mice (P < 0.01). Wild-type animals did not develop significant calcifications when exposed to vitamin D. Combined administration of vitamin D and calcium significantly accelerates Randall\u27s plaque formation in a murine model. This original model raises concerns about the cumulative risk of vitamin D supplementation and calcium intakes in Randall\u27s plaque formation

Peroxisome proliferator-activated receptor beta/delta exerts a strong protection from ischemic acute renal failure.

Ischemic acute renal failure is characterized by damages to the proximal straight tubule in the outer medulla. Lesions include loss of polarity, shedding into the tubule lumen, and eventually necrotic or apoptotic death of epithelial cells. It was recently shown that peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) increases keratinocyte survival after an inflammatory reaction. Therefore, whether PPARbeta/delta could contribute also to the control of tubular epithelium death after renal ischemia/reperfusion was tested. It was found that PPARbeta/delta+/- and PPARbeta/delta-/- mutant mice exhibited much greater kidney dysfunction and injury than wild-type counterparts after a 30-min renal ischemia followed by a 36-h reperfusion. Conversely, wild-type mice that were given the specific PPARbeta/delta ligand L-165041 before renal ischemia were completely protected against renal dysfunction, as indicated by the lack of rise in serum creatinine and fractional excretion of Na+. This protective effect was accompanied by a significant reduction in medullary necrosis, apoptosis, and inflammation. On the basis of in vitro studies, PPARbeta/delta ligands seem to exert their role by activating the antiapoptotic Akt signaling pathway and, unexpectedly, by increasing the spreading of tubular epithelial cells, thus limiting potentially their shedding and anoikis. These results point to PPARbeta/delta as a remarkable new target for preconditioning strategies

Performance of creatinine-based equations for estimating glomerular filtration rate changes over time

Item does not contain fulltextBACKGROUND: Glomerular filtration rate (GFR) is commonly used to monitor chronic kidney disease (CKD) progression, but its validity for evaluating kidney function changes over time has not been comprehensively evaluated. We assessed the performance of creatinine-based equations for estimating GFR slope according to patient characteristics and specific CKD diagnosis. METHODS: In the NephroTest cohort study, we measured GFR 5324 times by chromium 51-labeled ethylenediamine tetraacetic acid renal clearance in 1955 adult patients with CKD Stages 1-4 referred to nephrologists (Stages 1-2, 19%) and simultaneously estimated GFR with both the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD) equations for isotope dilution mass spectrometry traceable creatinine; absolute and relative GFR slopes were calculated using a linear mixed model. RESULTS: Over a median follow-up of 3.4 [interquartile range (IQR) 2.0-5.6] years, the decline in mean absolute and relative measured GFR (mGFR) and CKD-EPI and MDRD estimated GFR (eGFR) was 1.6 +/- 1.2, 1.5 +/- 1.4 and 1.3 +/- 1.3 mL/min/1.73 m2/year and 5.9 +/- 5.3, 5.3 +/- 5.3 and 4.8 +/- 5.2%/year, respectively; 52% and 55% of the patients had MDRD and CKD-EPI eGFR slopes within 30% of mGFR slopes. Both equations tended to overestimate the GFR slope in the youngest patients and underestimate it in the oldest, thus producing inverse associations between age and mGFR versus eGFR slope. Other patient characteristics and specific CKD diagnoses had little effect on the performance of the equations in estimating associations. CONCLUSIONS: This study shows little bias, but poor precision in GFR slope estimation for both MDRD and CKD-EPI equations. Importantly, bias strongly varied with age, possibly due to variations in muscle mass over time, with implications for clinical care and research

Decrease in urinary creatinine excretion in early stage chronic kidney disease

NephroTest Study GroupInternational audienceBACKGROUND:Little is known about muscle mass loss in early stage chronic kidney disease (CKD). We used 24-hour urinary creatinine excretion rate to assess determinants of muscle mass and its evolution with kidney function decline. We also described the range of urinary creatinine concentration in this population.METHODS:We included 1072 men and 537 women with non-dialysis CKD stages 1 to 5, all of them with repeated measurements of glomerular filtration rate (mGFR) by (51)Cr-EDTA renal clearance and several nutritional markers. In those with stage 1 to 4 at baseline, we used a mixed model to study factors associated with urinary creatinine excretion rate and its change over time.RESULTS:Baseline mean urinary creatinine excretion decreased from 15.3 ± 3.1 to 12.1 ± 3.3 mmol/24 h (0.20 ± 0.03 to 0.15 ± 0.04 mmol/kg/24 h) in men, with mGFR falling from ≥ 60 to <15 mL/min/1.73 m(2), and from 9.6 ± 1.9 to 7.6 ± 2.5 (0.16 ± 0.03 to 0.12 ± 0.03) in women. In addition to mGFR, an older age, diabetes, and lower levels of body mass index, proteinuria, and protein intake assessed by urinary urea were associated with lower mean urinary creatinine excretion at baseline. Mean annual decline in mGFR was 1.53 ± 0.12 mL/min/1.73 m(2) per year and that of urinary creatinine excretion rate, 0.28 ± 0.02 mmol/24 h per year. Patients with fast annual decline in mGFR of 5 mL/min/1.73 m(2) had a decrease in urinary creatinine excretion more than twice as big as in those with stable mGFR, independent of changes in urinary urea as well as of other determinants of low muscle mass.CONCLUSIONS:Decrease in 24-hour urinary creatinine excretion rate may appear early in CKD patients, and is greater the more mGFR declines independent of lowering protein intake assessed by 24-hour urinary urea. Normalizing urine analytes for creatininuria may overestimate their concentration in patients with reduced kidney function and low muscle mass