Correction to: Therapeutic hypernatremia management during continuous renal replacement therapy with elevated intracranial pressures and respiratory failure.

The authors would like to report an error in the formula describing the correction factor for the protein content in the serum/plasma.

Therapeutic hypernatremia management during continuous renal replacement therapy with elevated intracranial pressures and respiratory failure.

Cerebral edema and elevated intracranial pressure (ICP) are common complications of acute brain injury. Hypertonic solutions are routinely used in acute brain injury as effective osmotic agents to lower ICP by increasing the extracellular fluid tonicity. Acute kidney injury in a patient with traumatic brain injury and elevated ICP requiring renal replacement therapy represents a significant therapeutic challenge due to an increased risk of cerebral edema associated with intermittent conventional hemodialysis. Therefore, continuous renal replacement therapy (CRRT) has emerged as the preferred modality of therapy in this patient population. We present our current treatment approach, with demonstrative case vignette illustrations, utilizing hypertonic saline protocols (3% sodium-chloride or, with coexisting severe combined metabolic and respiratory acidosis, with 4.2% sodium-bicarbonate) in conjunction with the CRRT platform, to induce controlled hypernatremia of approximately 155 mEq/L in hemodynamically unstable patients with acute kidney injury and elevated ICP due to acute brain injury. Rationale, mechanism of activation, benefits and potential pitfalls of the therapy are reviewed. The impact of hypertonic citrate solution during regional citrate anticoagulation is specifically discussed. Maintaining plasma hypertonicity in the setting of increased ICP and acute kidney injury could prevent the worsening of ICP during renal replacement therapy by minimizing the osmotic gradient across the blood-brain barrier and maximizing cardiovascular stability.

Impaired glucose metabolism - A potential risk factor for idiopathic nodular glomerulosclerosis: A single center study.

Nodular glomerulosclerosis is a characteristic histological finding of diabetic nephropathy (DN) with thickened glomerular basement membrane and hyalinized arterioles. Idiopathic nodular glomerulosclerosis (ING), a distinct clinicopathologic entity, is the term used to denote classic DN confirmed by light microscopy, immuno-fluorescence, and electron microscopy but in the absence of diabetes mellitus (DM). ING has been linked to heavy tobacco smoking, chronic hypertension, and obesity. We report the result of a retrospective study identifying seventeen subjects from Thomas Jefferson University (1999-2014) with biopsy-proven nodular glomerulosclerosis but no pre-existing history of DM. The main indications for percutaneous kidney biopsy (PKB) were either reduced renal function or the presence of proteinuria. The subjects' mean (±SD) age was 60.2 (14.4) years, their highest documented random glucose level was 104.4 (23.5) mg/dL, serum creatinine measured 2.35 (1.03) mg/dL, and body mass index calculated 29.4 (6.2) kg/m2. None of the patients fulfilled criteria for diabetes at the time of PKB. However, review of medical records revealed history of intermittently elevated blood glucose or borderline-high HgbA1c levels. The role of impaired glucose metabolism or insulin resistance, as a possible etiology for ING is potentially underestimated and needs additional studies.

Successful Practice Transitioning Between Hemodialysis and Hemodiafiltration in Outpatient Units: Ten Key Issues for Physicians to Remember.

Hemodiafiltration (HDF) during chronic renal replacement therapy (RRT) is a relatively new practice phenomenon, emerging over the last two decades. While the technological platforms utilized during chronic RRT are in many cases similar or effectively identical to conventional hemodialysis (HD), significant differences may emerge in daily practice. Several authors of this review moved practice site between the United States and the European Union and transitioned from an HD-based practice to predominantly HDF-practicing networks. In doing so, we became keenly aware of the potential pitfalls nephrologists may be facing during such transitions. This brief review is intended to provide a succinct overview of several practical concerns and complications nephrologists may encounter in daily practice of end-stage renal disease care, including but not limited to management of electrolytes, renal anemia and treatment goals and settings during HDF.

Targeted surgical parathyroidectomy in end-stage renal disease patients and long-term metabolic control: A single-center experience in the current era.

BACKGROUND: The long-term results of surgical parathyroidectomy (PTX) in end-stage renal disease (ESRD) patients are less well known in the modern era of newer activated vitamin-D analogs, calcimimetics and intraoperative monitoring of parathyroid hormone (PTH). METHODS: We performed a retrospective chart review of all ESRD patients undergoing PTX at the University of Mississippi Medical Center between January 2005 and August 2011, with follow-up data as available up to 4 years. All PTXs were performed with intraoperative second-generation PTH monitoring and targeted gland size reduction. RESULTS: The cohort (N = 37) was relatively young with a mean (±SD) age of 48.4 ± 13.9. 94.6% of the subjects were African American and 59.5% female. Preoperatively, 45.9% received cinacalcet (CNC) at a mean dose of 63.5 ± 20.9 mg. The size of the largest removed glands measured 1.7 ± 0.8 cm and almost all (94.6%) glands had hyperplasia on histology. The mean length of inpatient stay was 5.5 ± 2.4 days. Preoperative calcium/phosphorus measured 9.6 ± 1.2/6.6 ± 1.7 mg/dL with PTH concentrations of 1589 ± 827 pg/mL. Postoperative PTH values measured 145.4 ± 119.2 pg/mL. Preoperative PTH strongly correlated (P < 0.0001) with both alkaline phosphatase (ALP) levels (r: 0.596) and the number of inpatient days (r: 0.545), but not with CNC administration. Independent predictors for the duration of hospitalization were preoperative ALP (beta 0.469; P = 0.001) and age (beta -0.401; P = 0.005) (R2 0.45); for postoperative hypocalcemia, age (beta: -0.321; P = 0.006) and preoperative PTH (beta: 0.431; P = 0.036) were significant in linear regression models with stepwise selection. CONCLUSION: Gland-sparing PTX achieved acceptable control of ESRD-associated hyperparathyroidism in most patients from a socioeconomically challenged, underserved population of the United States.

Peritoneal dialysis: The unique features by compartmental delivery of renal replacement therapy.

Despite decades of research, the clinical efficacy of peritoneal dialysis (PD) remains enigmatic. We may wonder why the modality fail in some patients but perhaps the more proper question would be, why it works in so many? We know that the contribution of residual renal function (RRF), more so than in hemodialysis, is critically important to the well-being of many of the patients. Unique features of the modality include the relatively low volume of dialysate fluid needed to provide effective uremic control and the disproportionate tendency for both hypokalemia and hypoalbuminemia, when compared to hemodialysis. It is currently believed that most uremic toxins are generated on the interface of human and bacterial structures in the gastrointestinal tract, the intestinal biota. PD offers disproportionate removal of these toxins upon "first-pass", i.e., via PD fluid exchanges before reaching the systemic circulation beyond the gastrointestinal compartment. Studies examining the net removal gradient of protein-bound uremic toxins during PD are scarce, whereas RRF receives considerably more attention without effective interventions being developed to preserve it. We propose an alternative view on PD, emphasizing the modality's compartmental nature, both for its benefits and the limitations.

Symmetrical craniofacial hypertrophy in patients with tertiary hyperparathyroidism and high-dose cinacalcet exposure.

We are reporting on a series of two patients with end-stage renal disease on hemodialysis, presented for surgical parathyroidectomy secondary refractory hyperparathyroidism. Both patients had failed maximized medical managements, including higher-than-usual doses of the calcimimetic cinacalcet (270 and 180 mg/day, respectively). On physical exam, both patients had marked symmetrical craniofacial hypertrophy with coarse distortion of facial features, similar in appearance to past reports of Sagliker syndrome. On X-ray and computed tomographic exam, they had peculiar areas of bone absorption on the skull, imitating the radiologic appearance of multiple myeloma. Bone biopsy of the maxilla, however, did not show the expected brown tumor, but rather described only fibrosis and reactive bone formations. This phenotype developed while being on cinacalcet, progressed despite escalation of therapy, and improved only after parathyroidectomy. Both patients developed massive "hungry bone syndrome" after parathyroidectomy necessitating prolonged i.v. calcium infusion. This pattern of severe facial distortion likely represented an adverse consequence of severe tertiary hyperparathyroidism, along with supraphysiologic dose of cinacalcet administration and 25-hydroxy vitamin D deficiency in sensitive individuals. The genetic base of this observation remained unexplained.