Unilateral hydronephrosis and hypertension: cause or coincidence?

In the present study, the frequency and the mechanism of hypertension associated with unilateral hydronephrosis (UHY) were investigated in 115 patients. Hypertension (blood pressure greater than 140/90 mm Hg) was found in 20% of 101 consecutive patients with UHY. Twenty-six patients with UHY and hypertension were followed for 35 months and the effect of surgery on blood pressure was analyzed. Blood pressure fell from 178 +/- 4/108 +/- 4 to 135 +/- 2/84 +/- 2 mm Hg after surgery. Hypertension was cured in 62%, improved in 19% and unchanged in 19%. In 73% of the cured patients the PRA-ratio was greater than or equal to 1.5, while all unchanged patients had a value of less than 1.5. Hypertensive patients were significantly older than normotensive patients, but did not differ in kidney function, underlying cause of hydronephrosis, incidence of urinary tract infection or frequency of interstitial nephritis. We conclude that in UHY the incidence of hypertension is not particularly high. However, in a substantial number of patients, high blood pressure is reversible by surgery. In most of these patients the renin-angiotensin-aldosterone system seems to play an important role in sustaining high blood pressure, although in some patients other mechanisms might be operative as well. Since the overall incidence of hypertension is not particularly high in UHY, this secondary form of hypertension appears to be rare.

Renal vein immunoreactive renin in patients with renal artery stenosis and essential hypertension.

In 36 patients with unilateral renal artery stenosis and in 24 with essential hypertension the plasma levels of total immunoreactive renin, and enzymatically active renin were measured in both renal veins (V) and in the aorta (A) by direct RIA by using monoclonal renin antibodies. Active renin and trypsin-activatable inactive renin were also measured by indirect RIA with angiotensin-I antibodies. The V/A ratio for the different forms of renin calculated from the results of direct and indirect RIA were not different. The V/A ratio of active renin for the kidney with the stenotic artery was 3.04 +/- 0.28 (mean +/- sem) with direct and 3.02 +/- 0.25 with indirect RIA. The contralateral ratio was 1.04 +/- 0.02 with the direct and 1.05 +/- 0.02 with the indirect RIA. In essential hypertension it was 1.28 +/- 0.04 with direct RIA and 1.28 +/- 0.04 with indirect RIA. Chronic treatment with captopril had no influence on this ratio in both patients groups. The V/A ratio of total immunoreactive renin was lower than that of active renin and this ratio had lost discriminative power for lateralization. This ratio was significantly greater than one on the affected side in renal artery stenosis but not contralaterally and in essential hypertension. This study shows that renin activity after trypsin-activation of plasma is an accurate measure of the total renin concentration, i.e. active renin plus prorenin. It also shows that a kidney with a stenotic artery secretes inactive renin, which is immunologically related to active renin and is likely to be prorenin. Direct RIA for measuring active renin is technically more simple than indirect RIA. Direct RIA however is somewhat less sensitive. For measuring the V/A ratio for active renin in patients with renal artery stenosis this can be overcome by stimulating the renin-angiotensin system for instance by captopril.

Neuropeptide Y: a novel renal peptide with vasoconstrictor and natriuretic activity.

A novel vasoconstrictor peptide, neuropeptide Y (NPY), has been identified in considerable quantities in the renal artery and kidney. Within the kidney, NPY was confined to the cortex and corticomedullary interface, the regions where the juxtaglomerular apparatus is most numerous. In the isolated perfused rat kidney, NPY caused a prompt dose-dependent increase in perfusion pressure and reduction in flow, with only a small fall in glomerular filtration rate (GFR). In spite of the reduced renal perfusion, a dose-dependent natriuresis was observed. This response contrasts to the response of this preparation to noradrenaline, which causes sodium reabsorption. The presence of a potent vasoconstrictor and natriuretic peptide within the rat renovascular system suggests that it may play a significant role in the control of renal function.

Renal vein renin studies in renovascular hypertension--do they really help?

Measurement of the renal vein renin ratio (RVRR) is commonly used to predict the response of blood pressure to surgery in hypertensive patients with unilateral renovascular disease. We have reviewed our experience in 37 such patients in whom renal vein renin levels were measured basally and after stimulation of renin secretion with intravenous diazoxide or tilting. Twenty-four patients were cured or improved. When a basal ratio of greater than or equal to 1.5 (diseased: normal kidney) was taken as a positive test the false positive rate was 39% and the false negative rate 71%, there being little difference in outcome between those with ratios above or below 1.5. No other threshold value of RVRR identified those responding to surgery, and acute stimulation of renin secretion did not increase the value of the test. We conclude that the RVRR is of no prognostic value in the surgical treatment of hypertension due to unilateral renovascular disease.

Decreased fibrinolytic activity in vessels and ureters of rejecting human kidneys.

Plasminogen activator (PA) activity was determined with a histochemical fibrin slide technique in renal arteries, veins and ureters in 62 transplanted kidneys and again at transplantectomy in 12 transplants who later underwent irreversible rejection. At transplantation PA activity was the same whether the grafts later rejected or not. There was a significantly decreased PA activity in the vessels and ureters in rejected transplants. The role of the fibrinolytic system as a pathogenetic factor in rejected kidneys is discussed.

Segmental kidney resection in children with small, hypertension-producing intrarenal vascular lesions.

Renal angiography is indispensable in the study of children with suspected renal hypertension. Main or segmental renal artery stenoses are usually well-demonstrated by midstream abdominal aortography, but small intrarenal vascular abnormalities can be easily overlooked when such a nonselective method is used. Such tiny abnormalities, however, can be the cause for, or indication of focally increased renin production and consequent hypertension. The most common primary intrarenal lesions (stenoses, focal occlusions) may be readily apparent on good arteriograms. Quite often, however, they are angiographically occult, and their presence is indicated indirectly by tortuous or "corkscrew" intrarenal collaterals. The need for selective renal arteriograms and segmental renal vein renin assays in the work-up of such patients is stressed, and the effectiveness of treatment by segmental renal resection rather than nephrectomy in patients with such lesions is illustrated.

Renin secretion at the individual nephron level.

Blood was collected from the descending aorta, from a renal efferent arteriole and from the renal vein of a rat. The renin concentrations of the blood samples were measured. The renal vein renin concentration was 673 +/- 81 (SE) ng ml-1h-1 which was significantly higher than the concentration in the aorta of 456 +/- 50 (SE) ng ml-1h-1. The concentration of renin in the renal efferent arteriole was significantly lower than that in the aorta. These observations imply that net renin secretion is a combination of two processes; removal between artery and efferent arteriole and entry between efferent arteriole and renal vein. It appears that renin is released into the interstitium and enters the circulation at the capillary level rather than being released into the afferent or efferent arterioles. This mode of secretion supports the suggestion that the renin angiotensin system may primarily work intra-renally rather than through the systemic circulation.