Renal expression of AQP1 in the high-fat nutritional obesity of rat / Expresión renal de AQP1 en la obesidad nutricional alta en grasas en ratas

AQP1 plays an essential role in maintaining body water balance. In the kidney, AQP1 is localized to the apical and basolateral membrane of epithelial cells in the proximal tubule and descending thin limb of Ansa nephroni (Henle's loop) where it reabsorbs the vast majority of filtered water. The growing epidemic of obesity and metabolic diseases particularly obesity-related kidney disease is getting more and more attention in this century. However, a full understanding of mechanisms involved to the progressive renal disease is still unclear, in particular AQPs in the kidney of obesity. In this paper, we examined the localization of AQP1 in renal cortex and medulla of ND (normal diet) and HFD (high-fat diet) at rats. In the renal cortex and medulla, immunolight microscopy revealed weak expression of AQP1 in the apical and basolateral membrane of epithelial cells at the proximal straight/convoluted tubule of HFD compared with ND, respectively. The same result was confirmed in the thick descending limb and descending thin limb of Henle's loop. In the high-fat nutritional obesity of rats, decreased AQP1 levels may not directly cause serious obesity-related kidney disease, e.g. chronic kidney disease, even end-stage renal disease. But at least, AQPs (AQP1 in this study) was one of initially conditions to the incentive of obesity-related kidney disease.

Las acuoporinas tipo 1 (AQP1) constituyen una parte esencial en el mantenimiento del equilibrio del agua en el cuerpo. En el riñón, la AQP1 se localiza en la membrana apical y basolateral de las células epiteliales, en el túbulo proximal y en el segmento descendente del Ansa nephroni o asa nefrónica (asa de Henle), donde reabsorbe la gran mayoría de agua filtrada. La creciente epidemia de obesidad y enfermedades metabólicas en el siglo actual, hacen que la enfermedad renal relacionada con la obesidad esté recibiendo cada vez más atención. Sin embargo, aún no existe un conocimiento definitivo de los mecanismos implicados en la enfermedad renal progresiva, en particular los relacionados a las acuoporinas renales en la obesidad. En este trabajo, examinamos la localización de AQP1 en la corteza y la médula renales de la dieta normal (DN) y dieta alta en grasa (DAG) en ratas. En la corteza y médula renales, la microscopía de luz reveló una expresión débil de AQP1 en la membrana apical y basolateral de las células epiteliales en el túbulo contorneado proximal del grupo DAG en comparación con el grupo DN, respectivamente. El mismo resultado se confirmó en la porción descendente gruesa y en la porción descendente delgada del asa nefrónica. En ratas del grupo DAG, la disminución de los niveles de AQP1 pudo no ser la causa directa de una enfermedad renal grave relacionada con obesidad, como por ejemplo, enfermedad renal crónica, o una enfermedad renal terminal. No obstante, en este estudio, la expresión renal de AQP1 constituyó una de las condiciones iniciales para inducir la enfermedad renal relacionada con obesidad.

Expression of V2R and AQPs in the renal medulla of high-fat nutritional obesity of rat / Expresión de V2R y AQPs en la médula renal de ratas con obesidad nutricional alta en grasas

Recent evidence has indicated that adipose tissue produces bioactive substances that contribute to obesity-related kidney disease, altering the renal function and structure. Eight of the AQPs are expressed in the kidney, where several of them contribute to water absorption and maintenance of body water balance. In the study, we mainly examined the localization of AQP2, AQP3 and V2R in renal medulla of Normal Diet (ND) and High-fat Diet (HFD) of rats, respectively. In renal medulla of HFD, immunolight microscopy revealed weak expression of AQP2 at the apical plasma membrane and intracellular vesicles of principal cells of the IMCD and OMCD. AQP3 and V2R expression also observed a decrease in immunolabelling in the IMCD and OMCD. It was suggested that excess lipid accumulation may lead to lipotoxicity and may be the major driver of organ dysfunction such as water reabsorption dysfunction, which may be resulted from abnormal response of rphan G-protein-coupled receptors in kidney.

La evidencia reciente ha indicado que el tejido adiposo produce sustancias bioactivas que contribuyen a la enfermedad renal relacionada con la obesidad, alterando la función y la estructura renal. Ocho de los AQP se expresan en el riñón, donde varios de ellos contribuyen a la absorción de agua y al mantenimiento del equilibrio hídrico corporal. En el estudio, examinamos principalmente la localización de AQP2, AQP3 y V2R en la médula renal de ratas con dieta normal (ND) y ratas con dieta alta en grasas (HFD). En la médula renal del grupo HFD, la microscopía electrónica de barrido reveló una expresión débil de AQP2 en la membrana plasmática apical y las vesículas intracelulares de las células principales de IMCD y OMCD. La expresión de AQP3 y V2R también observó una disminución en el inmunomarcador en IMCD y OMCD. Se sugiere que el exceso de acumulación de lípidos puede conducir a lipotoxicidad y ser el principal impulsor de la disfunción orgánica, como la disfunción de reabsorción de agua, que puede ser el resultado de la respuesta anormal de los receptores acoplados a proteína rphan G en el riñón.

Tubulocystic carcinoma of kidney associated with papillary renal cell carcinoma.

Tubulocystic renal cell carcinoma (TCRCC) is a rare variant of renal cell carcinoma, which has distinct histology but there is some controversy about its association with papillary renal cell carcinoma (PRCC) and cell of origin in literature. We report an 18-year-old girl with the rare TCRCC of kidney associated with PRCC with metastases to the para-aortic nodes. The patient presented with hematuria and a right renal mass with enlarged regional nodes for which a radical nephrectomy with retroperitoneal lymph node dissection was done. On gross examination, a solid cystic lesion involving the lower pole and middle pole of the kidney measuring 12x9x9 cm was seen along with an additional cystic lesion in upper pole of kidney. Microscopically the main tumor showed the typical histology of a tubulocystic carcinoma with multiple cysts filled with secretions lined by variably flattened epithelium with hobnailing of cells. The mass in the upper pole was a high-grade PRCC and the nodal metastases had morphology similar to this component. To conclude, at least a small but definite subset of TCRCC is associated with PRCC, and cases associated with PRCC do seem to have a higher propensity for nodal metastasis as in the case we report.

The investigation of macrophage infiltration in the early phase of ischemic acute renal failure in mice

BACKGROUND/AIMS: Inflammation plays a key role in ischemic acute renal failure (ARF). The present study investigated the infiltration of macrophages in the early phase of ischemic ARF in mice. METHODS: Ischemic ARF was induced by renal clamping for 22 min, while the control mice underwent sham surgery (no clamping). The serum creatinine and blood urea nitrogen (BUN) levels were measured in the control and post-ischemia mice. Immunofluorescence staining was used to measure the number of CD 11b-positive cells in the kidney tissue sections to determine the amount of post-ischemic macrophage infiltration. Lipo-Cl2MBP (clodronate) for macrophages depletion was injected via a tail vein 5 d before ischemia induction and again 2 d before ischemia induction. RESULTS: The study found that the post-ischemia mice had higher levels of serum creatinine and BUN at 16 and 24 h compared to the controls. Immunofluorescence staining showed there were more macrophages in the post-ischemic tissue at 2, 8, 16 and 24 h compared to the control tissue, and that most of these macrophages were located in the outer medulla. The mice treated with clodronate prior to ischemia induction were found to have lower levels of serum creatinine compared to those mice that weren't treated with clodronate. CONCLUSIONS: There was significant infiltration of macrophages from the early phase of ischemic ARF, and this peaked at 16-24 h. Macrophage depletion using clodronate was protective against ischemic ARF.