Journal of Postgraduate Medicine
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Year : 1977  |  Volume : 23  |  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

Correspondence Address:
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;23:124-126

How to cite this URL:
Singh R K, Gupta D K, Singh R C. Adrenocortical function in renal hypertension. J Postgrad Med [serial online] 1977 [cited 2014 Apr 19 ];23:124-126
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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 [2],[3],[12],[13] their clinical implication is poorly under­stood. Plasma and urinary glucocorti­coids have been reported to be within normal limits in essential benign hyper­tension. [17] On the other hand altered clearance rate of 17-hydroxycorticoids have also been demonstrated in essential hypertension. [8] Similarly the role of aldosterone in metabolic alterations of malignant hypertension is well known. [9],[15] 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. [7] Appleby et a1, [1] Peterson et a1 [14] and Neher and Wettstein [11] 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.


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 [17] In hyperten­sive patients the levels of glucuronide conjugates of 17-OHCS are decreased and conversely the levels of sulfate con­jugates are elevated. [8] 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. [16] 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 [4] 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. [6] 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. [5],[9] Likewise an­other mineralocorticoid, i.e., 18-OH-DOC is also secreted more in hypertension. [10] 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.


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