Olivier Niel

Pediatric en bloc kidney transplantation into pediatric recipients: the French experience.

Afanetti M, Niaudet P, Niel O, Saint Faust M, Cochat P, Berard E. Pediatric en bloc kidney transplantation into pediatric recipients: The French experience. 
Pediatr Transplantation 2012: 16: 183–186.

Anemia in congenital nephrotic syndrome: role of urinary copper and ceruloplasmin loss.

To the editor: Mechanisms for anemia in patients with nephrotic syndrome (NS) are complex and incompletely understood. Copper is an essential mineral in red blood cell metabolism. It is absorbed in the intestine, bound to its carrier protein, transported to the liver, and stored. Up to 95% of serum

Fluid status evaluation by inferior vena cava diameter and bioimpedance spectroscopy in pediatric chronic hemodialysis

BackgroundEvaluation of patient’s dry weight remains challenging in chronic hemodialysis (HD) especially in children. Inferior Vena Cava (IVC) measurement was reported useful to assess fluid overload both in adults and children.MethodsWe performed a monocentric prospective study to evaluate the relation between predialytic IVC diameter measurements and hydration status evaluated by physicians and bioimpedance spectroscopy (BIS) and between IVC measurements and persistent hypertension.ResultsForty-eight HD sessions in 16 patients were analyzed. According to physicians, patients were overhydrated in 84.5% of dialysis sessions, 20.8% according to BIS, and 0%, 4.1% and 20.8% according to IVC inspiratory, expiratory and collapsibility index reference curves respectively. There was no correlation between relative overhydration evaluated by BIS and IVC measurements z-scores (p = 0.20). Patients whose blood pressure normalized after HD had a more dilated maximal IVC diameter before dialysis session than patients with persistent hypertension (median − 0.07SD [−0.8; 0.88] versus −1.61SD [−2.18; −0.74] (p = 0.03)) with an optimal cut-off of −0.5 SD.ConclusionsIn our study, IVC measurement is not reliable to assess fluid overload in children on HD and was not correlated with extracellular fluid volume assessed by BIS measurements. However, IVC measurements might be of interest in differentiating volume-dependant hypertension from volume-independant hypertension.

Is the renin-angiotensin system actually hypertensive?

The historical view of the renin–angiotensin system (RAS) is that of an endocrine hypertensive system that is controlled by renin and mediated via the action of angiotensin II on its type 1 receptor. Numerous new angiotensins (Ang) and receptors have been described, the majority being hypotensive and natriuretic, namely Ang-(1-7) and its receptor rMas. Renin and its precursor (pro-renin) can bind their common receptor. In addition to the production of Ang II, this receptor triggers intracellular effects. Given the control of renin production by intracellular calcium, calcium homeostasis is of particular importance. Ang-(1-12), which is not controlled by renin, is converted to several different angiotensin peptides and is a new pathway of the RAS. Local RAS enzymes produce or transform the different hyper- or hypotensive angiotensin within vessels and organs, but also in blood through circulating forms of the enzymes. In the kidney, a powerful local vascular RAS allows for the independence of renal vascularization from systemic control. Moreover, the kidney also contains an independent urinary RAS, which counterbalances the systemic RAS and coordinates proximal and distal sodium reabsorption. The systemic and local effects of renal RAS cannot be analyzed without taking into account the antagonistic effect of renalase. Our concept of RAS needs to evolve to take into account its dual potentiality (hyper- or hypotensive).

Artificial intelligence improves estimation of tacrolimus area under the concentration over time curve in renal transplant recipients

It has been shown that renal graft survival largely depends on the type and dosing of immunosuppressant treatments [1]. Tacrolimus, a widely-used calcineurin inhibitor, has a narrow therapeutic window, which makes regular drug monitoring necessary [2]. Interestingly, area-under-the-concentration over time curve (AUC) correlates better with clinical complications, such as nephrotoxicity [3], infections and acute rejection, compared to trough levels. This article is protected by copyright. All rights reserved.

Hypernatremia and acute pancreatitis in chronic kidney disease: back to the salt mines. Questions

BackgroundAcute pancreatitis can be a life-threatening complication in patients with chronic kidney disease (CKD), especially in kidney transplant recipients.Case diagnosis/treatmentThe patient was 7 years old when he received renal transplantation for CKD secondary to posterior urethral valves. Two years later, he presented with severe necrotizing pancreatitis (Ranson’s score 5, Balthazar’s score 8). Viral and genetic testing came back negative; pancreatitis was attributed to the patient’s treatments (prednisone, trimethoprim-sulfamethoxazole, and everolimus). Twenty days later, necrotized pancreatic cysts had formed. Two drains were surgically inserted into the abdomen, and continuous cyst lavage was started with normal saline solution. Two days later, blood tests revealed severe hypernatremia and hypokalemia. We suspected unwanted peritoneal dialysis had occurred because of the high sodium chloride content and the absence of potassium in the normal saline solution being used for cyst lavage. We switched to a peritoneal dialysis solution for the lavage, leading to complete correction of hydroelectrolytic disorders.ConclusionAcute pancreatitis is a frequent and potentially severe complication in CKD patients. It should be suspected in the presence of nonspecific symptoms, such as abdominal pain or vomiting. Rigorous monitoring of electrolytes is also mandatory for managing CKD patients with acute pancreatitis.