Diabetic patients develop hypoaldosteronism which frequently caused hyperkalemia and metabolic acidosis and diabetic hypoaldosteronism is associated with selective unresponsiveness of aldosterone to angiotensin II(A II), but mechanism of defect in A II stimulated aldosterone response still remain unclear.
To elucidate the mechanism of defect in A II stimulated aldosterone response and whether the defect was corrected by insulin treatment. author evaluated the responses of aldosterone production to A II, K+ and ACTH. I also evaluated the products of phospholipase C(PLC) and phospholipase D(PLD) activation important for increase of intracellular calcium and protein kinase C activation after A II activation in adrenal glomerulosa cells prepared from streptozotocin induced diabetic rats.
Two weeks after induction of diabetes by streptozotocin, rats were sacrificed by decapitation. The aldosterone production to A II, K+ and ACTH was measured by RIA. Inositol triphosphate(IP3) and diacylglycerol(DAG) generated by activation of PLC and phosphatidic acid(PA), phosphatidylethanol(PEt) and DAG generated by activation of PLD were measured by anion exchange column and thin layer chromatography.
1) Plasma renin activity and aldosterone level were not different among control rats, untreated and insulin treated diabetic rats.
2) basal, ACTH and K+-stimulated aldosterone production were similar in cells from the three groups(p>0.05), but A II stimulated aldosterone production was significantly decreased in cells from untreated diabetic rats compared with control and insulin treated diabetic rats(p<0.05).
3) A II-induced IP3, PA, PEt and DAG generation was similar among the three groups(p>0.05).
These results suggested that decreased A II-stimulated aldosterone response was present in glomerulosa cells from strepzptocin induced diabetic rats and reversed by insulin treatments. The main defect of altered A II response of zona glomerulosa might be located in the step distal to the activation of phospholipase.
, Kyung Jin Kim, Sung Chul Hong, Suk Hyung Kang, Ha Eung Song, Hye In Kim, Soo Hyun Kim, Hyun Jung Oh, Hye Won Kang, Seo Woo Kim, Min-A Yu, Dong-Ryeol Ryu, Kyu-Bok Choi, Duk-Hee Kang Blockers of renin-angiotensin system(RAS) including ACE inhibitor or ARB are one of the most frequently prescribed medications for the treatment of hypertension, heart failure and proteinuria. One of the major side effects of these RAS blockers is the deterioration of renal function, mainly due to a reduction of intraglomerular pressure. Therefore, close monitoring of renal function is recommended when RAS blockers are initially prescribed, especially for the patients with impaired renal function.
We report a patient who was transferred to our hospital due to the sudden development of oliguria and dyspnea after treatment for hypertension with ACEi and ARB. She was finally diagnosed as RAS blocker-induced acute renal failure with pulmonary edema complicated on congenital solitary kidney. After hemodialysis and conservative treatment, her renal function was recovered with maintenance of normal urine output.
This case highlights the necessity of the functional and structural evaluation of kidney to prevent the serious complication such as acute renal failure before the administration of ACEi and/or ARB.
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