Effect of D-alpha-tocopherol on tubular nephron acidification by rats with induced diabetes mellitus

The objective of the present study was to determine if treatment of diabetic rats with D-alpha-tocopherol could prevent the changes in glomerular and tubular function commonly observed in this disease. Sixty male Wistar rats divided into four groups were studied: control (C), control treated with D-alpha-tocopherol (C + T), diabetic (D), and diabetic treated with D-alpha-tocopherol (D + T). Treatment with D-alpha-tocopherol (40 mg/kg every other day, ip) was started three days after diabetes induction with streptozotocin (60 mg/kg, ip). Renal function studies and microperfusion measurements were performed 30 days after diabetes induction and the kidneys were removed for morphometric analyses. Data are reported as means ± SEM. Glomerular filtration rate increased in D rats but decreased in D + T rats (C: 6.43 ± 0.21; D: 7.74 ± 0.45; D + T: 3.86 ± 0.18 ml min-1 kg-1). Alterations of tubular acidification observed in bicarbonate absorption flux (JHCO3) and in acidification half-time (t/2) in group D were reversed in group D + T (JHCO3, C: 2.30 ± 0.10; D: 3.28 ± 0.22; D + T: 1.87 ± 0.08 nmol cm-2 s-1; t/2, C: 4.75 ± 0.20; D: 3.52 ± 0.15; D + T: 5.92 ± 0.19 s). Glomerular area was significantly increased in D, while D + T rats exhibited values similar to C, suggesting that the vitamin prevented the hypertrophic effect of hyperglycemia (C: 8334.21 ± 112.05; D: 10,217.55 ± 100.66; D + T: 8478.21 ± 119.81æm²). These results suggest that D-alpha-tocopherol is able to protect rats, at least in part, from the harmful effects of diabetes on renal function.

Malnutrition as an additional risk factor to gentamicin nephrotoxicity / Desnutrição como um fator de risco adicional na nefrotoxidade à gentamicina

A relação entre a desnutrição e as doenças infecciosas tem sido descrita há algum tempo. A gentamicina é um antibiótico aminoglicosídeo muito utilizado no tratamento de infecções graves por gram-negativos, apesar de sua nefrotoxidade. Estudos experimentais e clínicos também mostraram alterações importantes na função renal durante a desnutrição. Assim sendo, o objetivo do presente estudo foi verificar se o uso da gentamicina (G) em ratos submetidos à restrição alimentar (R) pode interferir no desenvolvimento da nefrotoxidade à gentamicina. Ratos Wistar machos com dois meses de idade foram submetidos à restrição alimentar (50 porcento) durante 30 dias. Nos 10 últimos dias, eles foram tratados com soro fisiológico ou gentamicina (40mg/kg/dia intraperitoneal). Os grupos estudados foram: C)- ratos com alimentação ad libitum + soro fisiológico, G)- alimentação ad libitum + gentamicina, R)- restrição alimentar + soro fisiológico, RG)- restrição alimentar + gentamicina. Uma queda significativa na taxa de filtração glomerular (TFG) foi observada nos grupos R (5,69 ± 0,22) e G (5,31 ± 0,27) se comparados ao grupo C (7,17 ± 0,42 ml.min kg). No grupo RG, a diminuição a TFG foi mais evidente do que nos grupos G ou R, (4,42 ± 0,24 ml.min-1.kg-1). Em todos os grupos experimentais, a diminuição da TFG ocorreu paralelamente à diminuição do fluxo plasmático renal (FPR), de modo que a fração de filtração (FF porcento) foi mantida. Um declínio na proporção inulina urina/plasma foi observado em ambos os grupos tratados com gentamicina e também no grupo com restrição alimentar. Apesar de G e R "per se" causarem um aumento na excreção de Na elevado a +, os valores mais altos foram obtidos no grupo RG. Apesar do nosso estudo ter sido realizado num modelo experimental, se extrapolado a protocolos humanos pode-se sugerir que o uso de antibióticos aminoglicosídeos nos pacientes desnutridos deve ser feito com cautela, especialmente devido a função renal e considerando o risco aumentado potencial exibido por estes pacientes.

Effect of thyroparathyroidectomy on urinary acidification in diabetic rats

In previous studies we have shown stimulation of renal acid excretion in the proximal tubules of rats with diabetes of short duration, with no important alterations in glomerular hemodynamics; on the other hand, in thyroparathyroidectomized rats (TPTX model), a significant decrease in renal acid excretion, glomerular filtration rate (GFR) and renal plasma flow (RPF) was detected. Since important changes in the parathyroid hormone-vitamin D-Ca axis are observed in the diabetic state, the present study was undertaken to investigate the renal repercussions of thyroparathyroidectomy in rats previously made diabetic by streptozotocin (45 mg/kg). Four to 6 days after the induction of diabetes (DM), a group of rats were thyroparathyroidectomized (DM + TPTX). Renal functional parameters were evaluated by measuring the inulin and sodium para-aminohippurate clearance on the tenth day. The decrease in the GFR and RPF observed in TPTX was not reversed by diabetes since the same alterations were observed in DM + TPTX. Net acid (NA) excretion was unchanged in DM (6.19 ± 0.54), decreased in TPTX (3.76 ± 0.25) and returned to normal levels in DM + TPTX (5.54 ± 0.72) when compared to the control group (6.34 ± 0.14 µmol min-1 kg-1). The results suggest that PTH plays an important vasodilator role regarding glomerular hemodynamics, since in its absence the impairment in GFR and RPF was not reversed by the diabetic state. However, with respect to acid excretion, the presence of diabetes was able to overcome the negative stimulus represented by TPTX

The renal effects of kainic acid

the respone of juvenile cultivated Piaractus mesopotamicus to handling stress, whthout anesthesia, was determined over 3-5 min (T1), 1 h (T2) and 6 h (T3) afeter capture. Plasma cortisol, glucose and total cholesterol were measured. Hyperglycemia present at T2 continued to rise until T3 while plasma cortisol levels increased but were similar at T2 and T3. Total plasma cholesterol was altered only at T3. Hyperglycemic changes were greater in fish without than stomach contents during the T2-T3 period. These differences in hyperglycemic changes may reflect the role of hormones other than cortisol in the regulation of glucose release in these fish