Moderate hyperosmolar hyponatremia caused by excessive off-label use of icodextrin during peritoneal dialysis.

Icodextrin use during the long dwell of a peritoneal dialysis (PD) regimen is commonly used to increase ultrafiltration. Its use may cause a mild and clinically insignificant degree of hyponatremia. We describe a patient who was admitted twice to our medical center on an atypical continuous ambulatory peritoneal dialysis (CAPD) regimen utilizing solely icodextrin with 2 exchanges (12-hour dwells). On both admissions, he had hyperosmolar hyponatremia in the 120-mmol/L range with a large osmolal gap. After icodextrin was stopped and his PD prescription was switched to dextrose solutions, both hyponatremia corrected and the osmolal gap quickly disappeared. The accumulation of osmotically active solute in extracellular fluids results in efflux of water from the cellular compartment and produces both hyponatremia and hypertonicity [1]. This tonic effect occurs most frequently with hyperglycemia, but other substances can also cause this, including mannitol, sorbitol, glycine, and maltose [1, 2]. In this report, we present a patient with end-stage renal disease (ERSD) on an atypical off-label PD regimen utilizing solely icodextrin solutions who developed hyperosmolar hyponatremia in the 120-mmol/L range, with a large osmolal gap. This appeared to be due to absorbed metabolites of icodextrin, mainly maltose.

Acute Oxalate Nephropathy Caused by Excessive Vegetable Juicing and Concomitant Volume Depletion.

Acute oxalate nephropathy (AON) induced by high dietary intake of oxalate-rich food is a rare cause of acute kidney injury and end-stage renal disease (ESRD). We describe a 68-year-old man with adequate baseline renal function who developed severe AON and ESRD. Six months earlier, he started a daily oxalate-rich fruit and vegetable juice diet high in spinach, with a calculated daily oxalate dietary intake of 1500 mg, about 10 times a typical diet. Renal biopsy showed extensive tubular oxalate deposits and acute tubular damage; the renal tissue was relatively free of chronic changes such as glomerulosclerosis, tubular atrophy, and interstitial fibrosis. A year later, he remains dialysis dependent.

FGF23-Associated Tumor-Induced Osteomalacia in a Patient With Small Cell Carcinoma: A Case Report and Regulatory Mechanism Study.

Tumor-induced osteomalacia (TIO) is typically caused by phosphaturic mesenchymal tumor (PMT) that secretes the phosphaturic hormone, fibroblast growth factor-23 (FGF23), resulting in decreased phosphate reabsorption in kidneys, hypophosphatemia, and finally osteomalacia. Rare cases of malignant tumor manifesting with TIO other than PMT had been reported, although in most of these reports, except one, circulating FGF23 levels were not evaluated and tissue expressing of FGF23 was not confirmed. In this article, we report a case of TIO in a patient with pulmonary small cell carcinoma with liver metastasis. The patient manifested with hypophosphatemia. His circulating level of FGF23 was markedly increased. The expression of FGF23 in tumor cells was confirmed. Furthermore, the regulatory mechanism of FGF23 in this patient was also investigated.

Renal effects of high-dose celecoxib in elderly men with stage D2 prostate carcinoma.

AIM: To prospectively study the clinical renal effects of daily high-dose celecoxib, a COX-2 inhibitor, in a cohort of elderly sick men (mean age 74.5 years) with advanced prostate cancer. MATERIAL AND METHOD: 44 men with advanced hormoneresistant prostate cancer participated in oncologic Phase II trials. All received celecoxib 400 mg bid for a median 6 months. Monthly laboratory measurement and blood pressure were monitored, and all cases of acute kidney injury (creatinine > 50% above baseline) and hyperkalemia (potassium > 5.5 mmol/l) were evaluated. Mean chemistries, BP, and estimated GFR (e-GFR) during treatment were compared to 6-month periods before and after treatment. RESULTS: There was no change in e-GFR (pre, 78.1 ± 22 ml/min; during treatment, 76 ± 19 ml/min). Serum K rose (4.25 ± 0.4 mmol/l to 4.39 ± 0.3 mmol/l, p = 0.03), and bicarbonate fell (28.16 ± 0.2 to 26.18 ± 0.2 mmol/l, p < 0.01) with treatment. 15% of patients developed AKI, close to the incidence of AKI episodes in the pre- (9%) and post-treatment periods (13%). AKI was mild, short-lived, and reversible, except in a terminal patient who withdrew. All AKI occurred in states of renal hypoperfusion, and were not related to celecoxib alone. Hyperkalemia developed in 9% of patients. No patient developed new-onset proteinuria. CONCLUSION: High-dose celecoxib for 6 months was relatively well tolerated. e-GFR remained stable and there were minor electrolyte alterations. Although the AKI incidence was much higher than other studies, it was not much higher than in the pre- and post-treatment periods (high "background noise"). All AKI occurred in states of renal hypoperfusion, not unexpected for prostaglandin inhibitors.

Subglottic stenosis as a complication of Wegener's granulomatosis.

Wegener's granulomatosis (WG) is a relatively uncommon collagen vascular disease that can lead to both upper and lower airway disease. Subglottic stenosis is one manifestation of the airway disease and can occur even during the quiescent phase of the disease, independent of an active inflammatory response. A high index of suspicion is necessary for this complication in patients with known WG who complain of dyspnoea, and WG should be high on the differential diagnosis in those found to have "idiopathic" subglottic stenosis. We report the case of a patient who presented with this problem, and we review the prevalence, diagnosis, symptoms, and treatment.