Portal Vein Gas in a Diabetic Patient with Gas-forming Pararenal Abscess

The incidence of portal vein gas (PVG), which used to be an ominous sign of intestinal sepsis, has increased with progressive improvements in imaging modalities. Therefore, the clinical significance of PVG has changed. Emphysematous pyelonephritis (EPN) is a rare, potentially life-threatening and gas-forming infection of the renal parenchyma and/or its surroundings. Gas-forming pararenal abscess presenting with PVG is even rarer. We hereby present the case of a diabetic female with poor glycemic control, who was diagnosed to have EPN and PVG concurrently by computed tomography. She underwent percutaneous catheter drainage (PCD) of the pyelonephritis. Both cultures of blood and pus grew Klebsiella pneumoniae. Her subsequent clinical course was uneventful. In summary, EPN is a rare but potentially fatal urinary tract infection in diabetic patients, and finding PVG on computed tomography can aid in diagnosis. Conservative treatment with intravenous antibiotics and PCD of pus may be adequate for the patient with EPN. However, nephrectomy may be necessary if the patient deteriorates and PCD fails to contain the infection

The role of echocardiographic study in patients with chronic kidney disease

Despite the recent enormous advances in medicine, high mortality and morbidity rates among the chronic kidney disease (CKD) patients remain an important but unresolved issue. Cardiovascular disease is a major cause of mortality and morbidity in patients with CKD. Abnormal left ventricular geometry and functions are common in this patient group and have been proven to be correlated with a high cardiovascular mortality/morbidity and all-cause mortality. For this reason, echocardiographic study plays an important role in evaluating cardiac structure and functions as well as in stratifying prognostic risk. We here summarize the reported findings on the usefulness of echocardiographic methodologies and identify their roles in diagnostic and prognostic clinical approaches

Diuretics Prevent Thiazolidinedione-Induced Cardiac Hypertrophy without Compromising Insulin-Sensitizing Effects in Mice

Much concern has arisen regarding critical adverse effects of thiazolidinediones (TZDs), including rosiglitazone and pioglitazone, on cardiac tissue. Although TZD-induced cardiac hypertrophy (CH) has been attributed to an increase in plasma volume or a change in cardiac nutrient preference, causative roles have not been established. To test the hypothesis that volume expansion directly mediates rosiglitazone-induced CH, mice were fed a high-fat diet with rosiglitazone, and cardiac and metabolic consequences were examined. Rosiglitazone treatment induced volume expansion and CH in wild-type and PPARγ heterozygous knockout (Pparg+/−) mice, but not in mice defective for ligand binding (PpargP465L/+). Cotreatment with the diuretic furosemide in wild-type mice attenuated rosiglitazone-induced CH, hypertrophic gene reprogramming, cardiomyocyte apoptosis, hypertrophy-related signal activation, and left ventricular dysfunction. Similar changes were observed in mice treated with pioglitazone. The diuretics spironolactone and trichlormethiazide, but not amiloride, attenuated rosiglitazone effects on volume expansion and CH. Interestingly, expression of glucose and lipid metabolism genes in the heart was altered by rosiglitazone, but these changes were not attenuated by furosemide cotreatment. Importantly, rosiglitazone-mediated whole-body metabolic improvements were not affected by furosemide cotreatment. We conclude that releasing plasma volume reduces adverse effects of TZD-induced volume expansion and cardiac events without compromising TZD actions in metabolic switch in the heart and whole-body insulin sensitivity

Progression of stages 3b–5 chronic kidney disease—Preliminary results of Taiwan National Pre-ESRD Disease Management Program in Southern Taiwan

The outcomes and their predictors, and rates of estimated glomerular filtration rate (eGFR) changes among Taiwanese, an ethnic Chinese population, with chronic kidney disease (CKD) stages 3b–5, enrolled in a nationwide pre-end-stage renal disease (pre-ESRD) management program that have not been previously reported. Methods: This study focused on a cohort of patients enrolled in the Taiwan's pre-ESRD disease management program from Southern Taiwan, including 4061 CKD 3b–5 patients who received more than 12 weeks of follow-up from 2007 to 2010. The decline rates of eGFR, outcomes, and the predictors of initiating dialysis were analyzed. Results: The study participants consisted of patients who were 70.1 ± 12.3 years old, of whom 56.4% were male, 46.3% were diabetic, and 72.1% were hypertensive. The mean annual eGFR changes were 0.47 ± 0.42 mL/min/1.73 m2/year, −1.27 ± 0.32 mL/min/1.73 m2/year, and −2.69 ± 0.39 mL/min/1.73 m2/year for stages 3b, 4, and 5, respectively; however, more rapid declines were noted in diabetic patients. The Kaplan–Meier analyses revealed that the probabilities of patients remaining alive and free of dialysis treatment for CKD stage 3b, 4, and 5 without or with diabetes were 89.46% versus 84.65%, 79.88% versus 55.68%, and 34.42% versus 9.64%, respectively, during 42 months of follow-up. Male gender, diabetes, lower baseline eGFR, higher systolic blood pressure, lower hematocrit, and albumin levels were the significant risk factors for initiating dialysis. Conclusion: Even though we cannot conclude with certainty that the Taiwan pre-ESRD disease management program is beneficial in slowing the progression of CKD stages 3b–5, our preliminary results seem to suggest this trend. Furthermore, the program may be improved by integrating it with other programs, such as those on diabetes and hypertension, thus making it a more patient-centered, multidisciplinary program

Interleukin-19 mediates tissue damage in murine ischemic acute kidney injury.

Inflammation and renal tubular injury are major features of acute kidney injury (AKI). Many cytokines and chemokines are released from injured tubular cells and acts as proinflammatory mediators. However, the role of IL-19 in the pathogenesis of AKI is not defined yet. In bilateral renal ischemia/reperfusion injury (IRI)-induced and HgCl2-induced AKI animal models, real-time quantitative (RTQ)-PCR showed that the kidneys, livers, and lungs of AKI mice expressed significantly higher IL-19 and its receptors than did sham control mice. Immunohistochemical staining showed that IL-19 and its receptors were strongly stained in the kidney, liver, and lung tissue of AKI mice. In vitro, IL-19 upregulated MCP-1, TGF-β1, and IL-19, and induced mitochondria-dependent apoptosis in murine renal tubular epithelial M-1 cells. IL-19 upregulated TNF-α and IL-10 in cultured HepG2 cells, and it increased IL-1β and TNF-α expression in cultured A549 cells. In vivo, after renal IRI or a nephrotoxic dose of HgCl2 treatment, IL-20R1-deficient mice (the deficiency blocks IL-19 signaling) showed lower levels of blood urea nitrogen (BUN) in serum and less tubular damage than did wild-type mice. Therefore, we conclude that IL-19 mediates kidney, liver, and lung tissue damage in murine AKI and that blocking IL-19 signaling may provide a potent therapeutic strategy for treating AKI