Browsing by Subject "Proteinuria"

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    Age- and Sodium-Sensitive Hypertension and Sex-Dependent Renal Changes in Rats With a Reduced Nephron Number
    (American Heart Association, 2008-02-07) Salazar, Francisco; Reverte, Virginia; Saez, Fara; Lorai, Analia; Llinas, Maria Teresa; Salazar, F. Javier; Fisiología
    We have demonstrated that the reduction of angiotensin II effects during the nephrogenic period reduces the nephron number and induces the development of hypertension. The hypotheses examined are that this reduction of angiotensin effects leads to the development of an age-dependent sodium sensitive hypertension and that the hypertension is angiotensin II dependent. Newborn rats were treated with an angiotensin II type 1 receptor antagonist during the first 2 weeks of age. At 3 to 4 and 11 to 12 months of age, changes in systolic blood pressure, proteinuria, and renal function in response to a prolonged high sodium intake were examined. The basal blood pressure response to the administration of the angiotensin II receptor antagonist was also evaluated at both ages. Basal blood pressure was similarly elevated (P<0.05) in male and female treated rats, and the increment was age dependent. High sodium intake only elicited a blood pressure elevation (136±1 to 154±3 mm Hg; P<0.05) and a decrease in glomerular filtration rate (28%; P<0.05) at 11 to 12 months in treated rats. Blockade of angiotensin II receptors during renal development induced an increase (P<0.05) in proteinuria that was age and sex dependent, but high sodium intake only induced an elevation in proteinuria in the younger rats (50%; P<0.05). Hypertension was maintained by angiotensin II at both ages because blood pressure decreased to normal levels after treatment with an angiotensin II type 1 receptor antagonist. This study shows that the reduction of angiotensin II effects during the nephrogenic period modifies renal function and induces the development of an angiotensin II–dependent hypertension that becomes sodium sensitive during aging.
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    Evaluación de la proteinuria en perros con enfermedad de cusching, previo y posterior al tratamiento con ácido retinoico y ketoconazol.
    (Murcia, Universidad de Murcia, Servicio de Publicaciones, 2007) Martiarena, Beatriz; Madalena, Leticia; Mira, Graciela; Fidanza, Mercedes; Lalía, José; Ortemberg, Leonardo; Loiza, Mónica; Facultad de Veterinaria
    El hipercortisolismo ha sido señalado como causante de enfermedad renal por compromiso del compartimento glomerular. Su identifi cación precoz y no invasiva se realiza mediante el estudio cualitativo y cuantitativo de las proteínas urinarias, el primero evalúa el origen y el segundo la magnitud de las pérdidas. Estudios recientes proponen al ácido retinoico (AR) como una alternativa terapéutica efectiva en el Cushing de origen pituitario al uso de ketoconazol (Ktz) y otras drogas de acción antiesteroideogénica. El presente trabajo se realizó con el propósito de, evaluar la proteinuria en perros con hipercortisolismo pituitario dependiente (HPD), y determinar si la terapia con AR y ktz logran controlarla. Se estudió la proteinuria de 22 perros con HPD, 14 tratados con AR y 8 con Ktz, durante 6 meses. La determinación cuantitativa (técnica de Rojo de Pirogalol) mediante la relación proteína / creatinina urinaria (UP/C) determinó que, en 11/22 (50%) el valor fue anormalmente alto (= 0,51); en 3/22 (14%) dudoso y 8/22 (36%) tenían valores de proteinuria consideradas normal (< 0,3). El estudio cualitativo de la proteinuria (técnica SDS-PAGE) indicó que de los 11 perros con UP/C alta, 3/11 tenían proteinuria glomerular (27,3%), 6/11 glomérulo-tubular (54,54%), y 2 fi siológica o normal (18,18%). Los 3 perros con valores de UP/C dudoso tuvieron, 2 proteinuria glomerular, y 1 fi siológica por el SDS-PAGE. Un perro con UP/C fi siológica tenía proteinuria tubular por el método cualitativo. El total de perros con daño glomerular fue de 11 (50%). Los valores de UP/C persistieron al fi nal del estudio sin cambios notorios y la evaluación estadística entre tratamientos no indicó diferencias signifi cativas. Ningún perro con proteinuria normal evolucionó hacia la anormalidad, y aquellos que tenían la UP/C alta no modifi caron signifi cativamente los valores ni desarrollaron insufi ciencia renal. Se concluye que, al momento del diagnóstico, aproximadamente el 50 % de los perros con HPD tendrían daño glomerular, y que el tratamiento específi co del Cushing no logra controlar a la enfermedad renal.
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    Immunohistochemical analyses on serum proteins in nephrons of protein-overload mice by in vivo cryotechnique
    (Murcia : F. Hernández, 2007) Zhou, D.S.; Ohno, N.; Terada, N.; Li, Z.; Morita, H.; Inui, K.; Yoshimura, A.; Ohno, S.
    Immunohistochemical analyses on local distributions of serum proteins in living mouse kidneys are usually difficult to examine with conventional preparation methods. By using our “in vivo cryotechnique” combined with freeze-substitution, we have checked immunolocalizations of the serum proteins in nephrons of bovine serum albumin (BSA)-overload mice, and compared them with those obtained by the conventional preparation methods. In two days of daily BSA-injected mice, the immunolocalization of BSA could be observed in Bowman’s space and urinary tubules with their overt proteinuria, where another endogenous mouse albumin was similarly immunolocalized. The leakage of BSA and mouse albumin in Bowman’s space and their reabsorption into proximal tubules were detected in 55% of nephrons, where no leakage of immunoglobulin G1 (IgG1) was detected. However, the leakage of IgG1, in addition to BSA and mouse albumin, was detected in the other nephrons. By carefully examining immunolocalizations of BSA and IgG1, they were obviously different from those obtained by the conventional preparation methods without normal blood circulation into the kidneys. The immunolocalizations of both BSA and mouse serum proteins could be directly analyzed with the “in vivo cryotechnique”, suggesting that functional damage to glomerular filtration barriers are different at early stages of the BSA-overload mouse model, depending on each nephron of living mice.
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    Immunohistological score of transcription factor 21 had a positive correlation with its urinary excretion and proteinuria in immunoglobulin a nephropathy
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Takahashi-Kobayashi, Mayumi; Usui, Joichi; Yaguchi, Misa; Yamazaki, Satoshi; Kawamura, Tetsuya; Kaneko, Shuzo; Seshan, Surya V; Yamagata, Kunihiro
    Transcription factor 21 (TCF21) contributes to mammalian nephrogenesis, and especially to glomerular maturation. Our previous study suggested its influence on glomerular injury, showing that TCF21 expression in podocytes had a positive correlation with the urinary protein value and also with the urinary TCF21 concentration. We now focus on its influence on the clinical course of immunoglobulin A nephropathy (IgAN), as patients with IgAN constitute the largest population of individuals with primary chronic glomerulonephritis in the world. Twenty cases of IgAN were divided into two groups according to the immunohistological score (IHS) of glomerular TCF21 expression: group IHS1 (n=7) and group IHS2+3 (n=13). Sixteen of the 20 cases were followed up for 2 years. Group IHS2+3 had heavier urinary protein (p=0.03) and a greater urinary TCF21 level (p<0.001) compared to group IHS1 at baseline. None of the other factors including hematuria, estimated glomerular filtration rate (eGFR), or the Oxford classification showed a statistically significant difference between these two groups. At the 2-year follow-up, even though the rate of remission in urinary protein, hematuria and the eGFR decline were not statistically correlated to IHS, the IHS2+3 group had a slight tendency toward a steeper eGFR decline compared to IHS1 (p=0.31). The present study suggested that the higher IHS of TCF21 corresponded to heavier proteinuria and a higher urinary TCF21 level in IgAN. This could be the first step in determining the TCF21 value for predicting the prognosis for IgAN.