Urinary Kallikrein Activity in the Hypertension of Renal Parenchymal Disease

Mitas, John A.; Levy, Steven; Holle, Rolf; Frigon, Ronald P.; Stone, Richard A.

doi:10.1056/nejm197807272990402

Cited by 82 publications

(16 citation statements)

References 20 publications

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“…A recent report (17) from this same group did not note decreased urinary kallikrein excretion in either hypertensive white or black patients, though the number of patients studied (four ofeach race) was too small for adequate evaluation. These data are contrasted to other reports from Italy (19,28), Japan (18), and the United States (16,20,29) in which decreased urinary kallikrein was noted in hypertensive patients. The factors which may have led to these conflicts include: (a) racial differences, (b) assay differences, (c) comparison after stimulation with low sodium diet, and (d) inclusion ofpatients with essential hypertension and slight renal insufficiency.…”

Section: Discussioncontrasting

confidence: 99%

“…The reasons why some patients with primary aldosteronism do not have elevated urinary kallikrein excretion are not apparent. Acquired renal damage in some patients may decrease kallikrein excretion (20). This factor may have been of special importance in two (Nos.…”

Section: Discussionmentioning

confidence: 99%

“…The normal kallikrein response of black and white hypertensive patients with normal basal kallikrein excretion to potassium administration (17) also suggests that the renal kallikrein system is initially normal in essential hypertension. However, some investigators (19,20) have noted decreased urinary kallikrein excretion in white hypertensive patients even when glomerular filtration rate was normal. Inexplicably, one of these groups noted no significant difference in urinary kallikrein excretion in white normals vs. hypertensives during low sodium diet in other studies (16 …”

Section: Discussionmentioning

confidence: 99%

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Urinary Kallikrein Excretion in Essential and Mineralocorticoid Hypertension

Holland¹,

1980

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A B S T R A C T Urinary kallikrein excretion has been reported to be decreased in patients with essential hypertension and elevated in patients with primary aldosteronism as a reflection of mineralocorticoid activity. Low renin essential hypertension (LREH) has been postulated to result from excess production of an unknown mineralocorticoid(s ,ug/24 h for black normals) and a failure to achieve metabolic balance in 11/13 patients. Thus, the lesser kallikrein stimulation appeared to result from these two factors. Black and white hypertensives with creatinine clearance <80 ml/min had little increase in urinary kallikrein excretion with Florinef or low sodium diet.5 of 12 patients with primary aldosteronism or 17a-hydroxylase deficiency did not have an elevated urinary kallikrein excretion rate. Mild renal insufficiency may have contributed to this finding in two of these five patients. Nevertheless, this finding illustrates a limitation to the use of urinary kallikrein excretion rate as an index of mineralocorticoid activity. However, it appears that the majority of patients with LREH have no evidence for excess production of an unknown mineralocorticoid. The failure to find a decrease in urinary kallikrein excretion in racially matched patients with essential hypertension and normal renal function questions the postulate of a role of the kallikrein-kinin system in the initiation of essential hypertension.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Urinary Kallikrein Excretion in Essential and Mineralocorticoid Hypertension

Holland¹,

1980

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“…Urinary kallikrein excretion was decreased in hypertensive patients with mild renal insufficiency (152) and markedly decreased in those with reduced glomerular filtration rates, as in those with hypertension (153). Renal parenchymal diseases accompanied by hypertension, such as chronic glomerulonephritis, are associated with diminished urinary kallikrein activity (152).…”

Section: Urinary Kallikrein In Hypertensivesmentioning

confidence: 99%

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Katori

Murakami

2006

J Pharmacol Sci

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Abstract. It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them provides a satisfactory explanation. We propose, on the basis of accumulated data, that the reduced activity of the kallikrein-kinin system in the kidney may provide this link. Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron. Bradykinin generated is immediately destroyed by carboxypeptidase Y-like exopeptidase and neutral endopeptidase, both quite independent from the kininases in plasma, such as angiotensin converting enzyme. The salt-sensitivity of the blood pressure depends largely upon ethnicity and potassium intake. Interestingly, potassium and ATP-sensitive potassium (K ATP ) channel blockers accelerate renal kallikrein secretion and suppress blood pressure rises in animal hypertension models. Measurement of urinary kallikrein may become necessary in salt-sensitive normotensive and hypertensive subjects. Furthermore, pharmaceutical development of renal kallikrein releasers, such as K ATP channel blockers, and renal kininase inhibitors, such as ebelactone B, may lead to the development of novel antihypertensive drugs.

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“…6^6 Such a marked decrease in urinary kallikrein occurred in the absence of a change in aldosterone and may have resulted from a structural or a functional alteration in distal tubular cells, which are the main site of kallikrein synthesis and release. 35 A decreased urinary excretion rate of kallikrein has been observed in hypertensive patients with renal parenchymal disease 37 and at least some subjects with essential hypertension and no obvious renal functional alteration. 38 In fact, a diminished renal production of kallikrein could account for many of the renal abnormalities associated with CsA toxicity.…”

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confidence: 99%

Renal changes associated with cyclosporine in recent type I diabetes mellitus.

et al. 1991

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The effects of cyclosporine A treatment on arterial pressure and renal function were assessed in 11 young patients with type I diabetes of short duration. Cyclosporine was started at 7.5 mg/kg/day, progressively decreased to 6 3 mg/kg/day at 6 months, and then continued at a lower dose (4.1 mg/kg/day) for an additional 3 months in patients in whom remission of insulin dependency was obtained (n=6). After 3 months of cyclosporine, a slight but significant increase in arterial pressure (+5.2±1.5 mm Hg), a rise in renal vascular resistance (-20%), a decrease in glomerular filtration rate (-25%), and a fall in filtration fraction were observed. Such changes were sustained after 6 and eventually 9 months of therapy. The decrease in glomerular filtration rate observed during cyclosporine treatment contrasted with the lack of change in simultaneously estimated creatinine clearance; in fact, the creatinine clearance/ glomerular filtration ratio increased from 1.07±0.05% to 1.33±0.09% within 3 months of cyclosporine therapy, thus suggesting an enhanced tubular secretion of creatinine. Plasma renin activity and urinary excretion of kallikrein decreased significantly (-50%), whereas plasma aldosterone concentration remained unaltered and plasma concentration of potassium increased during cyclosporine therapy. These changes were observed in the presence of a constant urinary excretion of sodium and potassium and a constant body weight All parameters returned to pretreatment values within 3 months after cessation of cyclosporine. These results indicate that cyclosporine given for 6-9 months at a moderate dose causes a deleterious but reversible effect on arterial pressure and renal function in young diabetic patients. {Hypertension 1991;18:334-340)

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Urinary Kallikrein Activity in the Hypertension of Renal Parenchymal Disease

Cited by 82 publications

References 20 publications

Urinary Kallikrein Excretion in Essential and Mineralocorticoid Hypertension

Urinary Kallikrein Excretion in Essential and Mineralocorticoid Hypertension

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Renal changes associated with cyclosporine in recent type I diabetes mellitus.

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