Extrarenal Wilms' tumor (EWRT) is a rare entity, but primary bladder Wilm's tumor is even rarer with only 1 case reported. A 1-year old boy came with chronic urinary retention. Abdominal pelvic CT scan revealed intravesical mass arising from anterior bladder wall extending to the prostate and bladder neck. Initial cystoscopic diagnosis revealed chronic granuloma. We decided to perform partial cystectomy with final pathologic result of bladder Wilms' tumor. EWRT may occur in various organs, but primary bladder Wilms' tumor is extremely rare case.

Sepsis-associated overproduction of reactive oxygen species (ROS) and nitric oxide (NO) during pathogen infection leads to overwhelming oxidative stress, which has been recognized as a primary contributor to acute kidney injury (AKI). Hence, antioxidant therapy has been widely explored in order to find an effective treatment for sepsis-related AKI, in particular by using endogenous antioxidant – superoxide dismutase (SOD). We assessed the effect of oral SOD on the alteration of AKI biomarkers (creatinine and Neutrophil Gelatinase-Associated Lipocalin – NGAL) in endotoxin-induced septic murine. The animals were assigned as a healthy control, a septic control, and three treatment groups (250, 500, and 1000 IU oral SOD). Treatment of SOD was carried out by force-feeding for 16 weeks prior to intraperitoneal injection of lipopolysaccharide (LPS). The sepsis was assessed using the murine sepsis score (MSS) after 12 hours post-LPS injection, where the changes in plasma SOD, ROS, NO, creatinine, and NGAL were measured by enzyme-linked immunosorbent assay (ELISA). During sepsis, SOD was significantly decreased from its baseline level while other biomarkers were significantly increased (p<0.05) – except for NGAL. MSS exhibited a declining trend in SOD dosage-dependent manner, and was significantly different with that of septic control group at SOD dosage of 1000 IU (p<0.05). SOD treatment with a dosage as low as 250 IU could prevent the abnormal expression of the tested biomarkers during sepsis. There were significant reduction of plasma ROS, NO, creatine and NGAL in rats treated with 1000 IU SOD. Our study suggests the protective effect of SOD against sepsis-induced AKI by scavenging ROS and NO. Doi: 10.28991/ESJ-2022-06-02-06 Full Text: PDF

Sepsis is one of the leading causes contributing to the incidence of acute kidney injury (AKI). Oxidative stress can be used as the main approach against sepsis-induced AKI. One of the primary antioxidants that plays a role in warding off oxidative stress is superoxide dismutase (SOD). This research aimed to observe the effect of antioxidant SOD in inhibiting sepsis in AKI based on kidney tissue histopathology. The research method was an experimental laboratory with a post-test-only control group design. Twenty-five adult male rats aged 12–16 weeks, weighing between 200 and 250 g, were randomly divided into five groups: Group I, as a positive control, where rats were injected with lipopolysaccharides (LPS); Group II, as a negative control; Group III, as treatment 1, where rats were injected with LPS and administered orally with SOD (Glisodin®) 250 IU daily; Group IV, as treatment 2, where rats were injected with LPS and administered orally with SOD (Glisodin®) 500 IU daily; and Group V, as treatment 2, where rats were injected with LPS and administered orally with SOD (Glisodin®) 1000 IU daily. Rats were administered with SOD (Glisodin®) by oral gavage with a flexible feeding tube for 16 weeks, given once daily in the morning, and then injected with LPS of 10 mg/kg body weight. Glisodin SOD had a significant effect on murine sepsis score (MSS). MSS influenced the tubular injury score linearly. We conclude that the optimal dose of SOD at 1000 IU for inhibiting sepsis-induced AKI incidence is compared to SOD at a dose of 250 and 500 IU. The antioxidant effect of SOD can prevent sepsis-induced AKI with oxidative stress events.

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Abstrak. Periodik paralisis hipokalemia menyebabkan kelemahan otot yang progresif terutama pada kelompok otot proksimal tungkai bawah, serangan akut dapat terjadi secara berulang. Serangan pertama biasanya terjadi antara usia 5 tahun dan 35 tahun, tetapi frekuensi serangan paling tinggi antara usia 15 dan 35 tahun.  Ditemukan kasus Periodik paralisis hipokalemia yang berulang pada anak laki laki usia 15 tahun. Semua hasil analisis gejala klinis dan pemeriksaan penunjang sangat mendukung untuk diagnosis periodik paralisis hipokalemia.Kata kunci: periodik paralisis hipokalemia, kelemahan otot, usia 15 tahunAbstract. Periodic paralysis of hypokalemia causes progressive muscle weakness especially in the proximal lower leg muscle groups, acute attacks may occur repeatedly. The first attacks usually occur between the ages of 5 and 35, but the frequency of attacks is highest between the ages of 15 and 35. A case of recurrent hypokalemia periodic paralysis was found in a boy aged 15 years. All the results of clinical symptom analysis and investigations are very supportive for the diagnosis of periodic hypokalemia paralysis. Key words: periodic hypokalemia paralysis, muscle weakness, age 15 years