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A D Cumming

Publications and source records attributed to A D Cumming.

50 records · Page 3Linked to original sources
PubMed1986

The renal response produced by nonhypotensive sepsis in a large animal model.

We describe an animal model of generalized sepsis, induced in the sheep by cecal perforation, which reproduces the high systemic flow and peripheral vasodilation seen in early human sepsis. Despite volume loading, animals demonstrate a fall in glomerular filtration rate, oliguria, low fractional sodium excretion, maintained urine osmolarity, and increased plasma renin activity. Histologically, kidneys show no consistent abnormality; overall the findings suggest volume contraction or hypoperfusion. This is contradicted, however, by maintained blood pressure and pulmonary capillary wedge pressure, increased cardiac output, and reduced peripheral resistance. Increased Fc lysozyme and low molecular weight proteinuria suggest tubular damage. These paradoxical observations are currently unexplained.

Animals↗
PubMed1985

Haemodynamic and endocrine responses of the kidney to frusemide in mild essential hypertension.

Prostaglandin-dependent, frusemide-induced changes in renal plasma flow, glomerular filtration rate and plasma renin activity were measured in 14 patients with mild essential hypertension. The renal haemodynamic responses to frusemide were the same as in 10 normal subjects. Frusemide-induced changes in urinary PGE and kallikrein excretion were also the same as in normal subjects. Impaired renal release of vasodilator prostaglandins in essential hypertension is likely to be secondary to the hypertension rather than an underlying factor in its development.

Adult↗
PubMed1985

Urinary kallikrein and systemic prostacyclin synthesis during sodium chloride infusion in normal man.

An intravenous infusion of 3 litres of sodium chloride solution (saline: 150 mmol/l) was given over 1 h to normal subjects. During and immediately after the infusion, renal plasma flow increased in the majority of subjects, but the rise was not statistically significant. Significant increases in urine flow, sodium excretion, urinary kallikrein excretion and urinary excretion of dinor-6-keto prostaglandin (PG) F1 alpha, a measure of systemic PGI2 synthesis, were noted. Plasma renin activity and plasma protein concentration were significantly lowered by the infusion. At 2 h after the end of the infusion, although urine flow fell significantly, sodium excretion had not decreased. The reduction in plasma renin activity and plasma proteins persisted, and excretion of kallikrein and the PGI2 metabolite returned to control values. Overall, urinary kallikrein excretion correlated significantly with urine flow and with sodium excretion. Peak kallikrein excretion occurred in the second 30 min of the infusion, and preceded maximal urine flow and sodium excretion. The results suggest that increased systemic synthesis of PGI2 occurs in response to an acute infusion of sodium chloride, and may be an adaptive response of the vasculature to volume expansion. They support a role for the renal kallikrein-kinin system in the early diuretic and natriuretic response to saline infusion; the reduction in plasma renin activity and plasma protein concentration may be involved in both the early response and the persistent natriuresis 2 h after the infusion.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Intrinsic sympathomimetic activity of cardioselective beta-adrenoceptor blockers and effects on renal function.

The effects of a 21 infusion of isotonic sodium chloride on renal haemodynamics and sodium excretion were measured in nine normotensive volunteers. Changes in these responses to volume expansion induced by cardioselective beta-adrenoceptor blockade by drugs with (epanolol) and without intrinsic sympathomimetic activity (atenolol) were examined. Renal plasma flow was significantly lower before, during and after sodium chloride infusion whilst on treatment with atenolol compared with epanolol. Urinary sodium excretion was lower on atenolol than epanolol. Glomerular filtration rate was unchanged by either drug. Basal urinary kallikrein excretion was diminished by atenolol and both epanolol and atenolol inhibited the rise in urinary kallikrein excretion after sodium chloride infusion. Although some of these findings may be due to a more potent hypotensive effect of atenolol, intrinsic sympathomimetic activity may contribute to the apparent protective effects of epanolol on renal function.

Adrenergic beta-Antagonists↗
PubMed1985

Urinary kallikrein excretion in glomerulonephritis and nephrotic syndrome.

To assess the possible role of the renal kallikrein-kinin system in the pathogenesis of glomerulonephritis (GN), 24 h urinary kallikrein excretion (Uka) was measured in normal controls and in 32 patients with GN, 16 of whom had nephrotic syndrome. Compared with controls, Uka was decreased in GN without nephrotic syndrome (4.6 +/- 2.8 nkat day-1, controls 11.5 +/- 3.5 nkat day-1) but was markedly increased in patients with nephrotic syndrome (26.7 +/- 9.9 nkat day-1). The increased kallikrein excretion in nephrotic syndrome was not explained by leakage from plasma, protein binding of active kallikrein, passive 'washout' due to changes in sodium and water excretion, or by increased activity of the renin-angiotensin-aldosterone system, but may relate to changes in extracellular volume, plasma oncotic pressure and volume, or other intrarenal haemodynamic or hormonal factors. Increased activity of the renal kallikrein-kinin system is not a uniform finding in glomerulonephritis, but may be an important aspect of nephrotic syndrome.

Adolescent↗
PubMed1984

The plasma kallikrein kinin system in severely ill and traumatised patients.

Serial estimations of plasma prekallikrein in four critically ill patients in intensive care showed reduced values in each case, suggesting activation of the plasma kallikrein kinin system. In contrast, samples taken early from 15 patients attending an accident and emergency department with multiple trauma showed significantly elevated plasma prekallikrein concentrations; the significance of this observation is at present unclear.

Adult↗
PubMed1976

Significance of urinary C3 excretion in glomerulonephritis.

The third component of complement (C3) was measured in the urine of 98 patients with a variety of renal diseases. Renal biopsy was performed on 83 of the patients and examined by light, electron, and immunofluorescence microscopy. Urinary C3 was detected in cases of membranous glomerulonephritis, mesangiocapillary glomerulonephritis, rapidly progressive glomerulonephritis, and renal amuloidosis. It was not detected in minimal lesion glomerulonephritis; in cases of proliferative glomerulonephritis it was detected only in those showing histological evidence of a progressive lesion. Concentrations were low or undetectable in cases of non-immunological renal diseases. There was a good correlation between urinary C3 concentrations and the deposition of C3 in glomerular capillary walls, as seen by immunofluorescence microscopy, and there was no correlation with the degree or selectivity of proteinuria. Urinary C3 excretion appears to be an accurate indicator of continuing activity of disease. It is suggested that the presence of C3 in urine is due to complement fixation by immune complexes in glomerular capillary walls, and that urinary C3 estimations have potential applications in the study of glomerulonephritis.

Biopsy↗
PubMedDate not supplied

Urinary kallikrein excretion in chronic renal failure: relationship to blood pressure and the acute effect of captopril.

Previous studies of the renal kallikrein-kinin system in chronic renal failure (CRF) have given conflicting results. We have assessed activity of this vasoactive hormone system in CRF and investigated a possible relationship to hypertension in patients with CRF: 24-hour urinary kallikrein excretion (UKa) was measured in 22 patients with CRF (9 normotensive and 13 hypertensive) and 11 healthy controls. Age, sex, urine volume, and urinary sodium excretion were similar in each group. Compared with controls, UKa was reduced in both normotensive and hypertensive patients with CRF, with no difference between CRF groups. The reduction in UKa in CRF was less than the reduction in glomerular filtration rate (GFR), as assessed by endogenous creatinine clearance (CCr). When UKa was divided by CCr, UKa/mL CCr was therefore increased, to a similar extent, in both normotensive and hypertensive patients with CRF. This suggests that release of renal kallikrein from functioning nephrons is increased in CRF. The results do not support a role for deficient kallikrein release in the genesis of hypertension in CRF, as previously suggested; however, these abnormalities could be relevant to other aspects of renal function in CRF. The converting-enzyme inhibitor, captopril, was given to 5 patients with CRF, hypertension, and low UKa. Introduction of captopril was followed by a further reduction in UKa in all subjects. Captopril is known to inhibit kininase II, the principal enzyme involved in degradation of kinins; this potentiating effect may be counteracted by a reduction in renal kallikrein release and hence in kinin generation.

Adult↗