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|Year : 1977 | Volume
| Issue : 3 | Page : 124-126
Adrenocortical function in renal hypertension
RK Singh, DK Gupta, RC Singh
Department of Human Metabolism, Chest Diseases and Pharmacology, L.L.R.M. Medical College, Meerut, India
R K Singh
Department of Human Metabolism, Chest Diseases and Pharmacology, L.L.R.M. Medical College, Meerut
Adrenocortical functions in terms of urinary 17-ketosteroids (17-KS), 17-ketogenic steroids (17-KGS); 17-hydroxycortico steroids (17-OHCS) and aldosterone levels have been evaluated in 25 renal hypertensive patients in the present study. Urinary 17-KS, 17-KGS and 17-OHCS were within normal limits; however, aldosterone was elevated markedly in all the patients of renal hypertension. Thus, it appears that there exist a relation between this salt retaining steroid and renal hypertension.
|How to cite this article:|
Singh R K, Gupta D K, Singh R C. Adrenocortical function in renal hypertension. J Postgrad Med 1977;23:124-6
| :: Introduction|| |
The exact relationship between the adrenocortical steroids and the pathogenesis of hypertension is not clearly known. Although the available experimental evidence tends to suggest the importance of steroids in the production and maintenance of hypertension ,,, their clinical implication is poorly understood. Plasma and urinary glucocorticoids have been reported to be within normal limits in essential benign hypertension.  On the other hand altered clearance rate of 17-hydroxycorticoids have also been demonstrated in essential hypertension.  Similarly the role of aldosterone in metabolic alterations of malignant hypertension is well known. , However, little is known about urinary corticosteroids in renal hypertension.
Therefore in the present study an attempt was made to evaluate adrenocortical function in terms of urinary 17-ketosteroids (17-KS), 17-ketogenic steroids (17-KGS), 17-hydroxycorticosteroids (17-OHCS) and aldosterone levels in renal hypertensive patients.
| :: Material and Methods|| |
Twenty five patients of renal hypertension were selected for the evaluation of adrenocortical function in the present study. The ages of these patients ranged between 25 and 65 years. Some of these patients were admitted for treatment of some or the other type of nephrourinary diseases like chronic urinary tract infection or pyelonephritis. However, the criteria of diagnosis in these patients were: (1) evidence of hypertension without any cardiovascular or endocrinal disease, (2) clinical evidence of acute or chronic urinary tract infection supplemented with microscopic and culture studies of urine, (3) presence of varying degrees of renal in-absence of any clinical feature suggestive of adrenocortical dysfunction. 24hour urine sample of each patient was collected and subjected for the estimation of 17-KS, 17-KGS, 17-OHCS and aldosterone levels using standard procedures a, described by King and Wootton.  Appleby et a1,  Peterson et a1  and Neher and Wettstein  respectively. In these cases all medications were withdrawn 4 days before investigating the adrenocortical function. Similar studies were simultaneously carried out on 20 normal controls.
| :: Results|| |
The results of the estimations of urinary 17-KS, 17-KGS, 17-OHCS and aldosterone levels in 20 controls and 25 hypertensive patients are presented in [Table 1].
Urinary 17-KS and 17-OHCS levels were found to be within the normal limits and the mean values were 7.1 mg/ 24 hours (SE ± 0.58) and 3.9 mg/24 hours (SE ± 0.27) respectively. Further, we noticed a slight increase in urinary 17-KGS in these patients (mean 15.0 mg/24 hours, SE ± 1.2) though the difference was insignificant (p > 0.05). However, a marked increase (p < 0.001) in urinary aldosterone levels was observed in patients of renal hypertension with an average excretion of 10.6 µg/24 hours (SE - 1.9) [Table 1].
| :: Discussion|| |
In the present study renal hypertensive patients exhibited no change in urinary 17-KS and 17-OHCS levels. The urinary 17-KGS excretion was slightly increased in these patients though the difference was not significant as compared with the normals. Similar to the present study unchanged urinary excretion of cortisol and its metabolites in hypertension has been reported.  In hypertensive patients the levels of glucuronide conjugates of 17-OHCS are decreased and conversely the levels of sulfate conjugates are elevated.  However, in the present investigation the conjugation pattern of 17-OHCS has not been studied. Other studies have also demonstrated normal production rate of cortisol in cases of hypertension.  Presumably normal production of cortisol in such situations might be responsible for unchanged urinary corticoid levels observed in the present and similar other studies.
Further, we noticed marked increase in urinary aldosterone levels in renal hypertensive patients in the present study. Genest et a1  have also reported increased levels of urinary aldosterone in patients of hypertension. Angiotensin administration increases the aldosterone levels and in hypertensive patients the angiotensin levels are known to be elevated.  Thus, the elevated levels of angiotensin might contribute to some extent in increasing the aldosterone levels in hypertensive patients. The aldosterone secretion rate is known to increase in hypertension. , Likewise another mineralocorticoid, i.e., 18-OH-DOC is also secreted more in hypertension.  The increased secretion rate observed consistently in the aforesaid studies may also account for elevated levels of urinary aldosterone noticed in the present study. Thus, it appears that the glucocorticoids are not involved in renal hypertension. However, aldosterone levels are largely influenced in such states.
| :: References|| |
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