Extrarenal prorenin and renin in anephric Patients

Konrads, A.; Hummerich, W.; Vlaho, M; Wambach, G.; Böttcher, W.; Meurer, K. A.

doi:10.1007/bf01476969

Cited by 3 publications

(1 citation statement)

References 43 publications

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“…Such a relationship may be due to any combination of the following factors: a changing pattern of activation prior to secretion from storage granules in juxtaglomerular cells; augmented intra vascular activation or simply a relatively fixed plasma level of inactive renin originating from the juxtaglomerular cell. Neither the present nor previous work can resolve these possibilities but because the major part of IPRC comes from the kidney [9,17] a change in its activation mechanism dur ing increased secretion seems most likely.…”

Section: Discussionmentioning

confidence: 65%

Changes in Active and Inactive Renin with Haemodialysis

Thatcher¹,

Whitworth

Skinner

1982

Nephron

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Active (A) and inactive (I) plasma renin concentrations (PRC) were examined during haemodialysis in relation to blood pressure and body weight changes. Patients had either one (n = 15) or two (n = 51) remnant kidneys in situ, or were anephric (n = 4). 6 of the two remnant kidney patients had non-functioning renal allografts. Inactive renin was activated by acidification. Renin assay was by enzyme kinetic technique using sheep substrate and angiotensin I radioimmunoassay. Cryoactivation during handling was excluded. For the whole patient group the proportion of IPRC was inversely related to APRC in pre-dialysis plasma (p < 0.001). APRC and IPRC did not change with heparinisation nor did activation of renin occur across the dialyser. Dialysis with up to 3 kg reduction in body weight did not consistently raise APRC or IPRC. Blood pressure was not significantly correlated with IPRC or APRC during dialysis. In all situations a high APRC was associated with a low IPRC: APRC ratio consistent with preferential secretion of the active form and/or consumption of the inactive renin zymogen.

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Section: Discussionmentioning

confidence: 65%

Changes in Active and Inactive Renin with Haemodialysis

Thatcher¹,

Whitworth

Skinner

1982

Nephron

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Effects of furosemide and orthostasis on active and inactive renin in normal and anephric man

Konrads¹,

Hummerich²,

Vlaho³

et al. 1981

Eur J Clin Investigation

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We investigated active and inactive (acid-activatable) plasma renin in anephric and in normal persons. In anephric patients (n = 15) plasma concentration of active and inactive renin was 1.15 +/-- 0.2 and 40.7 +/- 7.1 microunits ml, respectively; angiotensin II (n = 13) was 14.5 +/- 1.9 pg/ml. Furosemide (n = 10), 40 mg i.v., and upright posture (n = 8) did not change active or inactive renin in the anephric state. In normal men, furosemide (n = 9) within 15 min increased active renin from 29.9 +/- 5.8 to 82.4 +/- 14.8 microunits/ml (P less than 0.001), while inactive renin slightly but not significantly decreased from 136.3 +/- 29.9 to 121.1 +/- 19.2 microunits/ml; orthostasis (n = 15) within 4 h stimulated active renin (P less than 0.001) and slightly raised inactive renin (P less than 0.05). Both furosemide and orthostasis increased (P less than 0.001 each) the proportion of active renin in normal persons. Studies in one patient within 24 h after bilateral nephrectomy indicated half-life to be 30-60 min for active and 2-4 h for inactive renin. Thus, we detected low levels of active renin and considerable amounts of inactive renin and angiotensin II in anephric patients. Our data suggest that about 30% of inactive renin in normal plasma is of extrarenal origin. The stimulation of active renin by furosemide and orthostasis is bound to the presence of the kidney. Our studies provide indirect evidence that both manoeuvres may stimulate the conversion of inactive to active renin within the human kidney.

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Renin and Renin Inhibition in Anephric Man

Opsahl

Smith

Murray

et al. 1993

Clinical and Experimental Hypertension

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Renin activity appears to be present in low concentrations in the plasma of anephric humans but could be artifactual secondary to inadvertent activation of prorenin during specimen collection and handling or from a renin-like enzyme. We studied the effects of specimen collection, storage, different assay conditions, trypsin activation, and the renin inhibitor EMD 56133 (E Merck, Darmstadt) on plasma renin activity (PRA) in anephric man. PRA was detectable in all seven bilaterally nephrectomized (BNX) patients (0.2 +/- 0.1 ng AI/ml/hr, range 0.1-0.7) but was significantly lower than normals (2.4 +/- 0.3 ng AI/ml/hr, range 1.5-3.1, p = 0.001). PRA was not different in BNX whether blood samples were collected on ice or at room temperature and assayed immediately or whether samples were frozen and assayed several days later. Prolonged cold storage of samples and five freeze-thaw cycles over six to seven months did not significantly increase PRA in normals or anephrics. However, deliberate repeated freezing and thawing over the period of a single day increased PRA 4.1-fold in BNX and 1.6-fold in normals. Renin-like activity was also detected in BNX individuals using renin concentration determinations with either excess human or sheep angiotensinogen. The inhibition of renin activity (IC-50% = 3.16 x 10(-9) molar) by EMD 56133 was not different between BNX and normals. Thus, active renin is present in the plasma of anephric humans and does not result from the inadvertent activation of prorenin due to sample handling. Although the source of PRA in BNX is unknown, the enzyme appears functionally normal as evidenced by the dose-response to a single renin inhibitor.

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Extrarenal prorenin and renin in anephric Patients

Cited by 3 publications

References 43 publications

Changes in Active and Inactive Renin with Haemodialysis

Changes in Active and Inactive Renin with Haemodialysis

Effects of furosemide and orthostasis on active and inactive renin in normal and anephric man

Renin and Renin Inhibition in Anephric Man

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