No abstract available.
Acute-Phase Proteins/*urine ; Female ; Glomerulonephritis, IGA/*blood/*urine ; Humans ; Kidney/*metabolism ; Lipocalins/*blood/*urine ; Male ; Proto-Oncogene Proteins/*blood/*urine

PURPOSE: The present study was aimed to determine whether there exist an altered regulation of tubular transporters and nitric oxide system in the kidneys in maleic acid-nduced metabolic acidosis. METHODS: Male Sprague-awley rats were treated with maleic acid (2 mmol/kg, every 24 hours, intraperitoneally) for 2 days. Control rats were injected with saline. At 24 hours following the second injection, rats were killed by decapitation. Plasma HCO3-and anion gap were measured. The protein expression of type 3 Na+/H+ exchanger (NHE3), type 1 Na+:HCO3- cotransporter (NBC1), and aquaporin (AQP)-1 in the cortex of the kidneys was determined by Western blot analysis. In addition, the expression of isoforms of nitric oxide synthase (NOS) was determined. Contents of nitric oxide metabolites (nitrite/ nitrate, NOx) were also measured in urine by colorimetric assay. RESULTS: Plasma concentrations of HCO3- were significantly decreased following the treatment of maleic acid, while plasma anion gap was did not differ between the experimental and the control groups. In the experimental group, the protein expression of NHE3 was significantly increased in the cortex of the kidney although the expression of NBC1 was not altered significantly. The expression of inducible NOS (iNOS), endothelial NOS (eNOS), and neuronal NOS (nNOS) was significantly increased in the cortex of the kidney. Accordingly, urine NOx contents were increased in the experimental group. In contrast, the expression of AQP1 was not altered. CONCLUSION: These results indicated that upregulation of NHE3 and nitric oxide system may play a role in regulation of acid-ase balance.
Acid-Base Equilibrium ; Acidosis* ; Animals ; Blotting, Western ; Decapitation ; Humans ; Kidney* ; Male ; Neurons ; Nitric Oxide Synthase ; Nitric Oxide* ; Plasma ; Protein Isoforms ; Rats* ; Sodium-Bicarbonate Symporters ; Sodium-Hydrogen Antiporter ; Up-Regulation

Heart failure is the pathophysiological state characterized by ventricular dysfunction and associated clinical symptoms. Decreased cardiac output or peripheral vascular resistance lead to arterial underfilling. That is an important signal which triggers multiple neurohormonal systems to maintain adequate arterial pressure and peripheral perfusion of the vital organs. The kidney is the principal organ affected when cardiac output declines. Alterations of hemodynamics and neurohormonal systems in heart failure result in renal sodium and water retention. Activation of sympathetic nervous system, renin-angiotensin-aldosterone system and non-osmotic vasopressin release stimulate the renal tubular reabsorption of sodium and water. Dysregulation of aquaporin-2 and sodium transporters also play an important role in the pathogenesis of renal sodium and water retention.
Aquaporin 2 ; Aquaporins ; Arterial Pressure ; Cardiac Output ; Epithelial Sodium Channels ; Heart ; Heart Failure ; Hemodynamics ; Kidney ; Perfusion ; Renin-Angiotensin System ; Retention (Psychology) ; Sodium ; Sodium Chloride Symporters ; Sodium-Potassium-Chloride Symporters ; Sympathetic Nervous System ; Vascular Resistance ; Vasopressins ; Ventricular Dysfunction ; Water-Electrolyte Imbalance

Fungal infections are associated with the lowest incidence of post-operative infection following renal transplantation. These infections, however, are associated with a high mortality rate. A 58-year-old man who had received a kidney transplant presented with confused mental status. A brain computed tomography (CT) scan showed a 5.4 cm-sized, septate and thin-walled ring-enhancing lesion. The patient underwent aspiration and drainage of the brain lesion. Aspergillus fumigatus was stained in cultures of the aspirated material. Following surgery, the patient was treated with voriconazole for four months. After four months of anti-fungal treatment, the size of the brain abscess was decreased and serum creatinine was 1.5 mg/dL. Here, we present details of the case, which showed a favorable outcome with the combination of early surgery and voriconazol administration.
Aspergillosis ; Aspergillus fumigatus ; Brain ; Brain Abscess ; Creatinine ; Drainage ; Humans ; Incidence ; Kidney ; Kidney Transplantation ; Middle Aged ; Pyrimidines ; Transplants ; Triazoles

No abstract available.
Pyelonephritis*

No abstract available.
Acute Kidney Injury* ; Lipocalins* ; Neutrophils* ; Plasma* ; Renal Insufficiency, Chronic*

No abstract available.
Hydronephrosis*

BACKGROUND: Compared to the general population, patients with end-stage renal disease have more gastrointestinal symptoms and a higher prevalence of peptic ulcer. Risk factors for peptic ulcer disease in patients with end-stage renal disease, however, remain poorly defined. This study aims to better identify those risk factors. METHODS: We analyzed 577 patients with end-stage renal disease from 2004 to 2016. We excluded patients with life-threatening conditions. All patients underwent upper endoscopy. We analyzed patient medical records, medication history, and endoscopic findings. Independent sample t test, chi-square test, Fisher’s exact test, and multiple logistic regression analysis were used in statistical analyses. RESULTS: Of the 577 patients with end-stage renal disease, 174 had peptic ulcer disease (gastric or duodenal ulcer). Patients on hemodialysis had a higher prevalence of peptic ulcer disease than those on peritoneal dialysis. Patients with peptic ulcer disease had lower serum albumin level and higher blood urea nitrogen level than those without peptic ulcer disease. Positive scores on two or more nutritional indices (albumin, serum cholesterol, uric acid, and creatinine levels) were associated with peptic ulcer disease in end-stage renal disease. CONCLUSION: Hemodialysis, hypoalbuminemia, and multiple malnutrition indices were associated with the prevalence of peptic ulcer disease in patients with end-stage renal disease receiving dialysis.
Blood Urea Nitrogen ; Cholesterol ; Creatinine ; Dialysis ; Endoscopy ; Humans ; Hypoalbuminemia ; Kidney Failure, Chronic ; Logistic Models ; Malnutrition ; Medical Records ; Nutrition Assessment ; Peptic Ulcer ; Peritoneal Dialysis ; Prevalence ; Renal Dialysis ; Risk Factors ; Serum Albumin ; Uric Acid

A 44-year-old man with chronic alcoholism presented with seizure and loss of consciousness. He was diagnosed with alcoholic hepatic encephalopathy, and his neurologic symptoms recovered after lactulose enema treatment. His initial serum sodium level was 141 mEq/L. However, his mental state became confused after treatment with lactulose enema for five days, and his serum sodium level increased to 178 mEq/L. After five days of gradual correction of serum sodium level from 178 mEq/L to 140 mEq/L, the patient’s mental state recovered, but motor weakness in both limbs remained. Therefore, magnetic resonance imaging of the brain was performed. T2-weighted brain images showed bilateral symmetrical hyperintensities in the central pons, basal ganglia, thalami, hippocampi and unci, which were consistent with central pontine and extrapontine myelinolysis. We report a rare case of osmotic demyelination syndrome that occurred as a result of a rapid increase from a normal sodium level to hypernatremia caused by lactulose enema administered to treat alcoholic hepatic encephalopathy.