Antoine Bouquegneau

Anorexia Nervosa and the Kidney

Anorexia nervosa is a common psychiatric disorder that disproportionately affects adolescents and young adults and is associated with high rates of morbidity and mortality. Anorexia nervosa can affect the kidney in numerous ways, including increased rates of acute kidney injury and chronic kidney disease, electrolyte abnormalities, and nephrolithiasis. Additionally, the diagnosis and treatment of anorexia nervosa-associated kidney diseases are challenging, reflecting complications such as refeeding syndrome, as well as the limitations of serum creatinine level in this population to estimate kidney function and the psychosocial challenges inherent with treating systemic manifestations of psychiatric conditions. In this review, we discuss kidney diseases and kidney-associated conditions that occur in individuals with anorexia nervosa, summarizing many of the challenges in treating patients with this disease.

Modification of Diet in Renal Disease versus Chronic Kidney Disease Epidemiology Collaboration equation to estimate glomerular filtration rate in obese patients

BACKGROUND Obesity is a recognized risk factor for both the development and progression of chronic kidney disease (CKD). Accurate estimation of glomerular filtration rate (GFR) is thus important in these patients. We tested the performances of two creatinine-based GFR estimates, the Modification of Diet in Renal Disease (MDRD) and the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations, in an obese population. METHODS Patients with body mass index (BMI) > 30 kg/m(2) were included. The reference method for measured GFR (mGFR) was (51)Cr-EDTA (single-injection method, two blood samples at 120 and 240 min). Both indexed and non-indexed results were considered. Serum creatinine was measured using the IDMS-traceable compensated Jaffe method. Mean bias (eGFR-mGFR), precision (SD around the bias) and accuracy within 30% (percentage of estimations within 30% of mGFR) were calculated for both equations. RESULTS The population included 366 patients (185 women) from two different areas. Mean age was 55 ± 14 years, and mean BMI was 36 ± 7 kg/m(2). Mean mGFR was 56 ± 26 mL/min/1.73 m(2) (71 ± 35 mL/min without indexation). In the total population, mean bias was +1.9 ± 14.3 and +4.6 ± 14.7 mL/min/1.73 m(2) (P < 0.05), and accuracy 30% was 80 and 76% for the MDRD and CKD-EPI equations (P < 0.05), respectively. In patients with mGFR > 60 mL/min/1.73 m(2), mean bias was +4.6 ± 18.4 and +9.3 ± 17.2 mL/min/1.73 m(2) (P < 0.05), and accuracy 30% was 81 and 79% (NS) for the MDRD and CKD-EPI equations, respectively. CONCLUSIONS The CKD-EPI equation did not outperform the MDRD study equation in this population of obese patients.

Biomarkers and physiopathology in the cardiorenal syndrome.

Acute cardiorenal syndrome (CRS) corresponds to an association of acute heart failure and a worsening of renal function. The detection of acute kidney injury (AKI) unfortunately occurs at a late stage of CRS, leading to an increased mortality of the patients. In this review, we described the pathophysiology of CRS and discussed the potential interest of biochemical biomarkers (namely creatinine, cystatin C, NGAL, KIM-1, fatty acid binding protein, Nacetyl-β-D-glucosaminidase and IL-18) that could potentially help to detect AKI earlier and thus reduce the morbi-mortality of the patients suffering from CRS.

Bone Disease after Kidney Transplantation

Bone and mineral disorders occur frequently in kidney transplant recipients and are associated with a high risk of fracture, morbidity, and mortality. There is a broad spectrum of often overlapping bone diseases seen after transplantation, including osteoporosis as well as persisting high- or low-turnover bone disease. The pathophysiology underlying bone disorders after transplantation results from a complex interplay of factors, including preexisting renal osteodystrophy and bone loss related to a variety of causes, such as immunosuppression and alterations in the parathyroid hormone-vitamin D-fibroblast growth factor 23 axis as well as changes in mineral metabolism. Management is complex, because noninvasive tools, such as imaging and bone biomarkers, do not have sufficient sensitivity and specificity to detect these abnormalities in bone structure and function, whereas bone biopsy is not a widely available diagnostic tool. In this review, we focus on recent data that highlight improvements in our understanding of the prevalence, pathophysiology, and diagnostic and therapeutic strategies of mineral and bone disorders in kidney transplant recipients.

Sclerostin levels in CKD patients: an important, but not definitive, step on the way to clinical use

Sclerostin, an inhibitor of the Wnt signaling pathway, inhibits bone formation. In a study of vascular biopsies of patients undergoing kidney transplantation, Qureshi et al. demonstrate that circulating sclerostin levels are associated with vascular calcification (VC). This adds to an emerging body of literature implicating sclerostin as a key link between chronic kidney disease-mineral and bone disorder and cardiovascular disease. Some confounders of this association remain, and the mechanisms by which sclerostin promotes VC have yet to be elucidated.

Sclerostin and chronic kidney disease: the assay impacts what we (thought to) know.

Background Sclerostin, a 22-kDa protein secreted by osteocytes, acts as a potent inhibitor of osteoblast activity. In chronic kidney disease (CKD), sclerostin is a putative driver of the bone-vascular axis. However, large discrepancies between sclerostin assays have been described. Methods We compared four different assays [Biomedica (BM), TecoMedical (TE), R&D (RD) and MesoScaleDiscovery (MSD)] in an analytical study and addressed the question whether bioassay choice affects the correlation between circulating sclerostin and clinical and biochemical determinants. Circulating sclerostin levels were determined in 39 prevalent dialysis patients and 82 non-dialysis patients referred for glomerular filtration rate measurement. Results In the 82 non-dialysis patients, we observed large differences in median (interquartile range) sclerostin concentrations (in pg/mL): BM, 984 [interquartile range (IQR) 648]; TE, 629 (IQR 237); RD, 154 (IQR 84) and MSD, 36 (IQR 19). The concordance correlation coefficient between assays was poor (0.1-0.44). The same discrepancies were observed in dialysis patients. A significant negative rank correlation was found between glomerular filtration rate and sclerostin measured by BM and TE but not by MSD and RD. Associations between sclerostin and age, gender, weight or parathormone were also different according to the assay considered. Conclusions Clinical inference relating sclerostin levels found in the general, CKD and dialysis populations is largely influenced by the assay used to measure this biomarker.

The Case : Acute renal failure and refractory hyponatremia

Kidney International (2016) 90, 713–714 incontinence. He had neither abdominal pain nor vomiting. He had lost 3 kg during the preceding 2 weeks. He had a past coronary artery bypass surgery. His medications were clopidogrel, atenolol, and perindopril. On physical examination, his supine blood pressure was 105/55 mmHg, his heart rate 52 beats/min, and his temperature 35.5 C. Laboratory tests (Table 1) showed hyponatremia, slight hyperkalemia, and elevated creatinine and blood urea nitrogen levels. Arterial blood gas analysis revealed metabolic acidosis. His urine sodium level was very low. Ultrasound of the renal tract showed normal kidney morphology, with the bladder moderately distended. Stool cultures were positive for Campylobacter jejuni for which clarithromycin was initiated. The presumed diagnosis was pre-renal acute kidney injury from dehydration exacerbated by previous use of perindopril, in turn caused by intense diarrhea. The patient was treated accordingly by intravenous bicarbonate, PlasmaLyte (Baxter; Lessines, Hainaut, Belgium), and sodium chloride fluids, antibiotics, and dialysis when the serum urea nitrogen reached 199 mg/dl (Figure 1). The patient still had liquid diarrhea (daily stool volume of more than 1.5 kg/d), weight loss (2 kg lost until dialysis initiation), a systolic blood pressure below 100 mmHg, a refractory hyponatremia (lowest value of 112 mmol/l in spite of oral water restriction), and the development of hypokalemia (lowest value of 2.97 mmol/l). The removal of the originally placed urinary catheter was impossible because of recurrence of urinary retentionwhen doing so. The patient developed nausea and moderate abdominal pain.