[Renin activity of renal venous blood and separate kidney function in reno-vascular hypertension. Diagnostic and prognostic value].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Angiotensin converting enzyme (ACE) inhibitors has been suggested to halt the progression of chronic renal failure. As the initial step of a controlled trial of this hypothesis, it was investigated whether start of enalapril in patients with severe chronic nephropathy might cause a critical fall in their renal function. Thirty-one patients were studied, 26 on chronic antihypertensive treatment with drugs other than ACE inhibitors and 5 untreated normotensive. 51Cr-EDTA plasma clearance and renal technetium-99m dimercaptosuccinic acid (99mTc-DMSA) scintigraphy were made before and 24 h after start of enalapril, mean dose 9 mg. Blood pressure fell from median 148/88 to 119/78 mmHg (p less than 0.01). Glomerular filtration rate (GFR) fell from median 14 to 12 ml/min/1.73 m2 (p less than 0.01). The median change in GFR was -14% (range -44% to +10%). The split renal function was unchanged and the scintigrams showed no intrarenal activity defects. In conclusion, enalapril caused a fall in GFR, which was clinically acceptable in most of the patients.
During the last 5 years we have followed nonoperatively all neonates with unilateral hydronephrosis and suspected ureteropelvic junction obstruction, regardless of the degree of hydronephrosis, shape of the diuretic renogram washout curve or initial degree of functional impairment. Of 104 patients 7 (7%) ultimately required pyeloplasty for obstruction, which was defined as a greater than 10% reduction in differential glomerular filtration rate and/or progression of hydronephrosis. Pyeloplasty returned renal function to pre-deterioration levels in all kidneys. In 16 patients with profound hydronephrosis and initial differential renal function less than or equal to 40% all traditional diagnostic tests for assessing obstruction, including diuretic renography washout pattern, were inaccurate in diagnosing obstruction and predicting which kidney would deteriorate. In 15 of 16 poorly functioning hydronephrotic kidneys rapid improvement in absolute and per cent differential renal function was observed, and the level of initial differential renal function served as a useful guide for timing of further diagnostic studies. Unilateral neonatal hydronephrosis appears to be a relatively benign condition and the risk of developing renal obstruction appears relatively slight. Because of diagnostic inaccuracy, the low risk of developing obstructive injury and the fact that many newborn kidneys with hydronephrosis rapidly improve function and dilation, it appears safe to follow neonatal unilateral hydronephrosis closely and nonoperatively.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Inhibition of the angiotensin converting enzyme (ACE) is associated with a decrease in renal vascular resistance, an increase in renal blood flow and a redistribution of intrarenal blood flow toward juxtamedullary nephrons. In general, ACE-inhibition does not affect normal glomerular filtration rate (GFR) but may increase GFR in patients on a low sodium intake prior to treatment. Since the rise in GFR is smaller than the rise in renal blood flow, in most instances a decrease in filtration fraction will result. In contrast to other vasodilator drugs, the decrease in blood pressure induced by ACE-inhibition is not accompanied by sodium retention, but rather by an initial natriuresis. ACE-inhibition also prevents secondary aldosteronism and thereby avoids renal potassium loss. The initial positive potassium balance after ACE-inhibition may protect patients with heart disease from potentially hazardous arrhythmias. Redistribution of intrarenal blood flow with increased medullary flow, in addition, will antagonize the hydrosmotic effect of vasopressin and thus result in a rise in free-water clearance. Finally, based on experimental evidence, long-term treatment with ACE-inhibitors may have a protective effect on renal function by reducing glomerular filtration pressure.