Antibiotic availability for outpatient treatment of acute peritonitis in chronic peritoneal dialysis patients: A case series.

Background: Peritoneal dialysis (PD) is a commonly used form of renal replacement therapy for patients that have reached end-stage renal disease. Acute bacterial peritonitis (ABP) in chronic PD patients results in pain, increased costs, injury to the peritoneal membrane, and PD modality failure. Optimal antibiotic treatment of acute bacterial peritonitis (ABP) in chronic PD patients should be intraperitoneal, outpatient-based, appropriate, prompt, and uninterrupted.

Length of Interdialytic Intervals Affects Morbidity and Mortality in Chronic Haemodialysis Patients.

Background: Chronic in-center hemodialysis (HD) patients may experience more morbidity and mortality after the weekend. Since our Veterans Administration Hospital HD unit is closed on the weekend, non-traditional HD schedules were created. Some schedules contained a 4-day weekend compared to the usual 3-day weekend.

A nanoformulation containing a scFv reactive to electronegative LDL inhibits atherosclerosis in LDL receptor knockout mice.

Atherosclerosis is a chronic inflammatory disease responsible for the majority of cases of myocardial infarction and ischemic stroke. The electronegative low-density lipoprotein, a modified subfraction of native LDL, is pro-inflammatory and plays an important role in atherogenesis. To investigate the effects of a nanoformulation (scFv anti-LDL(-)-MCMN-Zn) containing a scFv reactive to LDL(-) on the inhibition of atherosclerosis, its toxicity was evaluated in vitro and in vivo and further it was also administered weekly to LDL receptor knockout mice.

Administer but Do Not Dispense: Effect of Change in Medication Handling by Nurses on Outcomes of Home Dialysis Patients.

Background: To come into compliance with South Carolina statute, we changed how nurses handle medications (antibiotics, erythropoietin [EPO], calcitriol and heparin) in our outpatient home dialysis clinic. Nurses continued to administer medications in the clinic but no longer dispensed medications for patients to take home; instead, medications were dispensed from pharmacies to the patients by mail. We hypothesized that the abovementioned change in medication handling worsened clinical outcomes.

Angiotensin II receptors and peritoneal dialysis-induced peritoneal fibrosis.

The vasoactive hormone angiotensin II initiates its major hemodynamic effects through interaction with AT1 receptors, a member of the class of G protein-coupled receptors. Acting through its AT1R, angiotensin II regulates blood pressure and renal salt and water balance. Recent evidence points to additional pathological influences of activation of AT1R, in particular inflammation, fibrosis and atherosclerosis.

Clathrin-dependent internalization of the angiotensin II AT₁A receptor links receptor internalization to COX-2 protein expression in rat aortic vascular smooth muscle cells.

The major effects of Angiotensin II (AngII) in vascular tissue are mediated by AngII AT1A receptor activation. Certain effects initiated by AT1A receptor activation require receptor internalization. In rat aortic vascular smooth muscle cells (RASMC), AngII stimulates cyclooxygenase 2 protein expression.

Stimulation of Cyclooxygenase 2 Expression in Rat Peritoneal Mesothelial Cells.

Objective: Since peritoneal dialysis causes peritoneal fibrosis, we examined how glucose (osmotic factor), mannitol (osmotic control), and angiotensin II (AngII) regulate proinflammatory cyclooxygenase 2 (COX-2) in primary rat peritoneal mesothelial cells. Materials and Methods: For this study, we used the following material (n = 4-8 cell lines): cells, passages 1-2; I-AngII receptor surface binding (AT1R antagonist losartan, AT2R antagonist PD123319; both 10 µM); intracellular calcium probe calcium-5; COX-2 immunoblotting (β-actin normalized); real-time PCR of COX-2 gene PTGS2, and NF-κB inhibitor Ro-1069920 (5 µM). Results: AngII surface receptors were predominantly AT1R (minimally AT2R).

Angiotensin II activates NF-κB through AT1A receptor recruitment of β-arrestin in cultured rat vascular smooth muscle cells.

Activation of the angiotensin type 1A receptor (AT1AR) in rat aorta vascular smooth muscle cells (RASMC) results in increased synthesis of the proinflammatory enzyme cyclooxygenase-2 (COX-2). We previously showed that nuclear localization of internalized AT1AR results in activation of transcription of the gene for COX-2, i.e.

Peritonitis from Mycobacterium wolinskyi in a chronic peritoneal dialysis patient.

We report the case of acute peritonitis caused by a rapidly growing mycobacterium in a chronic peritoneal dialysis patient, whose renal failure had been caused by diabetic glomerulosclerosis. The organism cultured from the peritoneal dialysis fluid was Mycobacterium wolinskyi. Peritonitis caused by M.

Prerenal azotemia from excessive sweating in an adult with a cystic fibrosis gene mutation.

We present the case of a 58-year-old male with chronic kidney disease who was admitted to the hospital multiple times with extracellular fluid volume depletion and prerenal azotemia. Some episodes were associated with gastrointestinal fluid losses and others with profuse diaphoresis in the absence of gastrointestinal fluid losses. At the age of 57 years, a common cystic fibrosis transmembrane conductance regulator protein mutation and a family history of cystic fibrosis were documented.

Utility of percutaneous renal biopsy in chronic kidney disease.

Background: We tested the hypothesis that patterns of serum creatinine concentrations (S-cr) prior to percutaneous renal biopsy (PRB) predict the utility of PRB in safely making renal diagnoses, revealing treatable disease, and altering therapy in chronic kidney disease patients.

Methods: PRB specimens (170 patients) were assigned to 1 of 5 groups: S-cr never greater than 0.11 mM for at least 6 months prior to PRB (Group 1); S-cr greater than 0.

Angiotensin II-induced cyclooxygenase 2 expression in rat aorta vascular smooth muscle cells does not require heterotrimeric G protein activation.

Angiotensin II (AngII) initiates cellular effects via its G protein-coupled angiotensin 1 (AT(1)) receptor (AT(1)R). Previously, we showed that AngII-induced expression of the prostanoid-producing enzyme cyclooxygenase 2 (COX-2) was dependent upon nuclear trafficking of activated AT(1)R. In the present study, mastoparan (an activator of G proteins), suramin (an inhibitor of G proteins), 1-[6-[[17beta-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U73122; a specific inhibitor of phospholipase C), and sarcosine(1)-Ile(4)-Ile(8)-AngII (SII-AngII; a G protein-independent AT(1)R agonist) were used to determine the involvement of G proteins and AT(1A)R trafficking in AngII-stimulated COX-2 protein expression in human embryonic kidney-293 cells stably expressing AT(1A)/green fluorescent protein receptors and cultured vascular smooth muscle cells, respectively.

Thiol antioxidants regulate angiotensin II AT1 and arginine vasopressin V1 receptor functions differently in vascular smooth muscle cells.

Background: We compared the effects of the sulfhydryl-containing (thiol) antioxidant dithiothreitol (DTT), which disrupts disulfide bonds, on cell signaling through angiotensin II (AngII) Type 1 receptors (AT1Rs) and arginine vasopressin (AVP) V1 receptors (V1Rs). The AT1R contains two extracellular disulfides bonds but its ligand contains none, whereas the V1R contains no extracellular disufides bonds but its ligand contains 1.

Methods: We measured radioligand binding, intracellular calcium responses, and extracellular signal-regulated kinase phosphorylation in cultured rat aortic vascular smooth muscle cells and alterations in urine osmolality in intact rats.

COX-2 expression stimulated by Angiotensin II depends upon AT1 receptor internalization in vascular smooth muscle cells.

Previously, we demonstrated that nuclear localization of the Angiotensin II AT1A receptor was associated with the activation of transcription for the COX-2 gene, PTGS-2. The hypothesis of the present study is that AT1AR internalization from the plasma membrane is a first step in the nuclear localization of the endogenous AT1AR of rat aortic vascular smooth muscle cells and the resultant increase of COX-2 protein expression. Angiotensin II produced both a time- and concentration-dependent increase in COX-2 protein expression in these cells.