Blood pressure, renin-angiotensin system and urinary kallikrein in a case of juxtaglomerular cell tumor

Mimran, A; Leckie, Brenda J.; Fourcade, J; Baldet, Piérre; Navratil, H; Barjon, P

doi:10.1016/0002-9343(78)90780-5

Cited by 48 publications

(11 citation statements)

References 23 publications

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“…Peripheral vascular resistance would be expected to decrease exponentially following isolation of the tumour. The half-life of circulating renin is said to be between 39 and 100 min [11][12][13]. Measurement of this would require regular and frequent estimations of PRA, which we did not perform.…”

Section: Discussionmentioning

confidence: 99%

The anaesthetic management of a patient with a reninoma

Nicholson¹,

Rayman

Donaldson³

et al. 2003

Anaesthesia

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We report on the anaesthetic management of a 28-year-old woman presenting for excision of a reninoma. This is a very rare tumour of the juxtaglomerular cells of the kidney, which can be cured immediately by surgery. Previous reports have failed to record the presence or absence of perioperative cardiovascular lability. We have shown that blood pressure, cardiac index (CI) and systemic vascular resistance (SVRI) were remarkably stable in our patient throughout surgery, even during manipulation of the tumour. Isolation of the tumour was associated with a 23% reduction in SVRI, and a similar decrease in blood pressure. The cardiovascular lability associated with the removal of catecholamine-secreting tumours was not seen in this case.

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Section: Discussionmentioning

confidence: 99%

The anaesthetic management of a patient with a reninoma

Nicholson¹,

Rayman

Donaldson³

et al. 2003

Anaesthesia

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“…Renin release from the juxtaglomerular cell tumor has been reported to respond to changes in posture and/or in sodium intake [4,12]. Renin release in some cases has also been reported to increase after angiotensin converting enzyme inhibition, and decrease after n-blockade [4,13]. However, we recently reported one case of juxtaglomerular cell tumor that did not respond to these manuevers, including administration of the angiotensin II receptor antagonist, TCV-116 [7].…”

Section: Discussionmentioning

confidence: 99%

A Case of Renin-Producing Adrenocortical Cancer.

et al. 2000

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Abstract.Here we report a case of a renin-producing adrenocortical carcinoma. A 57-year-old woman was referred to our hospital complaining of thirst and generalized muscle weakness. She was diagnosed as being hypertensive and diabetic with associated hypokalemia and she had a hard elastic mass with a diameter of 10 cm on the left side of her neck. An abdominal computed tomography scan revealed a suprarenal mass on the left side (8.5 x 8 x 6.5 cm). Endocrinological examination demonstrated a marked elevation in the patient's serum glucocorticoid and sex steroid hormones as well as plasma renin activity. Histological examination of a sample taken from the neck mass revealed a metastasis from an adrenal carcinoma, which was stained positively with antibodies against cytochrome P450 and renin, establishing the diagnosis of a renin-producing adrenocortical carcinoma.Trilostane was effective in reducing serum cortisol levels, but mitotane was ineffective.

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“…Such a possibility is supported by the report that renin and kallikrein are in the same microsomal fraction of rat kidney extracts 38 and also by the observation that a patient with a renin-secreting tumor had very high urinary kallikrein excretion. 36 Although much more work is required to determine whether renal kallikrein converts inactive to active renin in vivo, its intrarenal location could interfere with the isolation of large molecular weight forms of renin from the kidney. Thus, Slater and Haber 37 found that the protease inhibitor PMSF, in combination with EDTA, dimercaprol and 8-OH quinoline, was required to preserve the large molecular weight form of renin in extracts of human kidney.…”

Section: Discussionmentioning

confidence: 99%

Activation of a prorenin-like substance in human plasma by trypsin and by urinary kallikrein.

Sealey¹,

Atlas²,

Laragh³

et al. 1979

Hypertension

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Correction of renal hypertension in the rat by prolonged infusion of angiotensin inhibitors. SUMMARY Inactive plasma renin (a prorenlp-like substance) can be activated by trypsin. There are also endogenous neutral serine proteases in plasma that can activate inactive renin in vitro, but only after protease inhibitors are either destroyed by acidification (the alkaline phase of acid activation) or inactivated by cold (cryoactivation). In the present study we have shown that cold also facilitates trypsin activation. But even at -4°C, as much as 1 rag/ral of trypsin was required to overcome endogenous inhibitors and reproducibly activate inactive plasma renin during a 1-hour incubation at pH 7.4. After partial destruction of plasma protease inhibitors by acidification to pH 33., less trypsin was required for complete activation at pH 7.4:200 Mg/ml at 25°C and 100 Mg/ml at -4°C. In contrast, 10 fig/ml of the renal enzyme urinary kallikrein completely activated inactive renin in previously acidified plasma at 25°C. Maximum activation of inactive plasma renin by either trypsin or renal kallikrein was almost identical. Both enzymes caused activation in plasmas deficient in Hageman factor or Fletcher factor (prekallikrein), suggesting that their ability to activate inactive renin is not mediated by these neutral serine proteases of the intrinsic coagulation system.Using maximum trypsin activation to define "total" renin, we found that among 22 normal subjects and hypertensive patients there was a direct relationship between the proportion of active renin in plasma (active/total) and the concurrent urinary kallikrein excretion (r = 0.46, p < 0.05). Normotensive white subjects had a higher proportion of active plasma renin than blacks, in whom urinary kallikrein is reported to be low. Altogether, these data suggest that there might be a link between prorenin and renal kallikrein in vivo. Further studies are required to evaluate this possibility and to determine whether prior hydrolysis of inactive renin, for example, by acidification, is required for renal kallikrein to activate inactive renin. 4 which seem to be completely inhibited.

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Blood pressure, renin-angiotensin system and urinary kallikrein in a case of juxtaglomerular cell tumor

Cited by 48 publications

References 23 publications

The anaesthetic management of a patient with a reninoma

The anaesthetic management of a patient with a reninoma

A Case of Renin-Producing Adrenocortical Cancer.

Activation of a prorenin-like substance in human plasma by trypsin and by urinary kallikrein.

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