Protein-energy wasting (PEW) is an important complication resulting from chronic kidney disease (CKD). Appetite impairment contributes significantly to PEW in these patients, but risk factors associated with having appetite impairment in patients with CKD remain elusive. Patients with an estimated glomerular filtration rate <60 mL/min/1.73 m² for ≥2 times at least three months apart were prospectively enrolled during 2017, with their demographic features, comorbidities, anthropometric parameters, physical and performance indices, functional status, frailty, sensory organ integrity, and laboratory data collected. Their appetite status was measured using the Council on Nutrition Appetite Questionnaire (CNAQ). We examined independent determinants of appetite impairment in these CKD patients using multiple regression analyses. Among 78 patients with CKD, 42.3% had CNAQ-identified impaired appetite. Those with an impaired appetite also had poorer physical performance, a higher degree of functional impairment, higher frail severities, lower serum sodium levels, less intact oral cavity, and a trend toward having less intact nasal structures than those without. Multiple regression analyses revealed that a higher frail severity, in the forms of increasing Study of Osteoporotic Fractures (SOF) scores (odds ratio (OR), 2.74; 95% confidence interval (CI), 1.15–6.57) and a less intact nasal structure (OR, 0.96; 95% CI, 0.92–0.995) were associated with a higher probability of having an impaired appetite, while higher serum sodium (OR, 0.76; 95% CI, 0.6–0.97) correlated with a lower probability. Based on our findings, in patients with CKD, the severity of frailty, serum sodium, and nasal structural integrity might modify appetite status. Therapies targeting these factors might be beneficial for appetite restoration in patients with CKD.

Renal tubulointerstitial lesions (TILs), a common pathologic hallmark of chronic kidney disease that evolves to end-stage renal disease, is characterized by progressive inflammation and pronounced fibrosis of the kidney. However, current therapeutic approaches to treat these lesions remain largely ineffectual. Previously, we demonstrated that elevated IL-36α levels in human renal tissue and urine are implicated in impaired renal function, and IL-36 signaling enhances activation of NLRP3 inflammasome in a mouse model of TILs. Recently, we synthesized NSC828779, a salicylanilide derivative (protected by U.S. patents with US 8975255 B2 and US 9162993 B2), which inhibits activation of NF-κB signaling with high immunomodulatory potency and low IC₅₀, and we hypothesized that it would be a potential drug candidate for renal TILs. The current study validated the therapeutic effects of NSC828779 on TILs using a mouse model of unilateral ureteral obstruction (UUO) and relevant cell models, including renal tubular epithelial cells under mechanically induced constant pressure. Treatment with NSC828779 improved renal lesions, as demonstrated by dramatically reduced severity of renal inflammation and fibrosis and decreased urinary cytokine levels in UUO mice. This small molecule specifically inhibits the IL-36α/NLRP3 inflammasome pathway. Based on these results, the beneficial outcome represents synergistic suppression of both the IL-36α-activated MAPK/NLRP3 inflammasome and STAT3- and Smad2/3-dependent fibrogenic signaling. NSC828779 appears justified as a new drug candidate to treat renal progressive inflammation and fibrosis.

We describe the case of a 62-year-old woman with schizophrenia and intellectual disability, who presented with intermittent muscle cramping for 2 weeks. A dysmorphic face and a positive Trousseau’s sign, but without ecchymosis or petechial lesion were noted. Laboratory data revealed impaired renal function (creatinine level = 1.6 mg/dL), severe hypocalcaemia (total calcium level = 5.7 mg/dL) with low urinary calcium excretion (13.2 mg/day), hyperphosphatemia (phosphate level = 7.3 mg/dL), and low intact parathyroid hormone level (52.5 pg/mL)—indicating primary hypoparathyroidism. A blood smear revealed thrombocytopenia (30,000 thrombocytes/µL) and giant platelets—indicating macrothrombocytopenia. Chromosome 22q11.2 deletion syndrome (22q11.2DS) in the deficient chromosome 22 was confirmed using multiplex ligation-dependent probe amplification showing haploinsufficiency in GP1BB and TBX-1. Cooccurrence of hypoparathyroidism and macrothrombocytopenia in 22q11.2DS is rare and can easily be misdiagnosed as idiopathic thrombocytopenia purpura and inappropriate splenectomy or chemotherapy can aggravate hypoparathyroidism. Early diagnosis of 22q11.2DS, characterized by hypoparathyroidism and macrothrombocytopenia, in elderly patients with schizophrenia can facilitate in avoiding circuitous diagnosis and inappropriate management.

Background: Empty sella syndrome is characterized by a constellation of symptoms that encompass various systems, and includes endocrine, neurologic, ophthalmologic, and psychiatric presentations. We here report a case of a young man presenting with severe hyponatremia due to empty sella syndrome and focus on changes in electrolytes during corticosteroid supplementation. Case report: A 36-year-old man presented with general weakness, poor appetite, and dizziness for 4 days. Physical assessment revealed lower limbs nonpitting oedema. Pertinent laboratory data showed severe hyponatremia (sodium 108 mmol/L). Endocrine work-up revealed low cortisol levels at 1.17 µg/dL (reference: 4.82–19.5 µg/dL) and inappropriately normal adrenocorticotropic hormone levels at 12.4 pg/mL (reference: 0.1–46.0 pg/mL), indicating secondary adrenal insufficiency. Brain magnetic resonance imaging confirmed the diagnosis of empty sella syndrome. He developed delirium and agitation one day after cortisol supplementation with a sodium correction rate of 10 mmol/L/day, while hypokalaemia (potassium 3.4 mmol/L) also developed. The symptoms improved after lowering the serum sodium level. This patient was eventually discharged after 12 days of hospitalization when the serum sodium and potassium levels were 139 mmol/L and 3.5 mmol/L, respectively. Conclusion: Herein, we address the importance of timely diagnosis of empty sella syndrome in patients with hyponatremia and highlight the close monitoring of the changes in electrolytes during corticosteroid replacement.