Search

Aim: To study effects of ACE inhibitors in patients with diffuse renal diseases at the stage of chronic renal failure (CRF)., Material and Methods: Acute changes in renal filtration and in renal hemodynamics in response to 100-200 mg captopril were studied in 7 patients with CRF and 6 patients with intact renal function. Effects of long-term ACE inhibitors were retrospectively studied in 50 patients with CRF (27 men, 23 women, mean age 46.0 +/- 1.9 years, 7 patients were over 60 years old). Sixteen patients were selected from this group who were followed up for a long time. They were examined for CRF progression rate when given conventional antihypertensive treatment and after treatment with ACE inhibitors., Results: Acute response to ACE inhibitors was the following: SCF fell by 18.4% on the average by the end on therapy week 1; by the end of week 3 renal hemodynamics showed stability, SCF returned to normal, effective renal plasm flow rose by 16.9%, serum potassium rose significantly after 7 days of treatment but did not reach 6 mmol/l. Effects of long-term ACE inhibitor in CRF: the treatment was discontinued after 30-60 days in 12 of 50 patients because of high creatinine (> 20%); in 38 patients ACE inhibitor had a pronounced antihypertensive and antiproteinuric action for 2-3 years, creatinine growth inhibited. Progression of CRF became slow., Conclusion: ACE-inhibitors in CRF had a nephroprotective effect but blood creatinine levels should be controlled especially within the first 1-2 months of treatment.

Aim: To study the role of abnormal intrarenal hemodynamics (IRHD) in progression of lupus nephritis (LN) and its response to therapy with inhibitors of angiotensin-converting enzyme (ACE)., Materials and Methods: The trial included 30 LN patients (27 females, 3 males; age 29.8+(-)10.4 years). 19 had aggravation of active LN. All the patients were free of chronic renal insufficiency. IRHD was studied with estimation of renal functional reserve (RFR) using protein loading, evaluation of clinical activity of LN and renal function, blood pressure. The tests were repeated after 6 months of treatment with ACE inhibitors (captopril and ramiprilol) in 13 patients (11 of them had exacerbation of active LN)., Results: Disturbed IRHD was found in 37% of the patients. Blood hypertension deteriorated this condition. Treatment with ACE inhibitors in 6 months brought about a significant decrease in blood pressure and improvement of IRHD. Before treatment RFR was absent in 46% of patients, after treatment in 1 patient., Conclusion: Defects in IRHD occur in LN frequently. These are related with the presence of blood hypertension and activity of LN. Inhibitors of ACE seem perspective in management of essential hypertension in LN patients but this hypothesis needs confirmation by the results of further studies.

The treatment with inhibitors of angiotensin-converting enzyme (ACE) was conducted in 57 patients with chronic diffuse renal diseases. Of them 45 patients received Capoten, 12 patients Renitek. ACE inhibitors were examined for effects on arterial pressure, proteinuria, renal and intrarenal hemodynamics. A hypotensive effect was apparent in hypertension and minimal in normotension. One month later renal bloodflow increased, glomerular filtration rate did not change. ACE inhibitors proved able to correct intrarenal hypertension: renal functional reserve returned to normal on posttreatment month 1-3 in 10 of 16 patients. Noticeable antiproteinuria effect of the drugs emerged 3 months after the treatment.

Antiproteinuria effects of angiotensin-converting enzyme (ACE) inhibitors was studied in 23 patients with chronic nephritis (CN) and 32 patients with diabetic nephropathy (DN). CN patients received Capoten, DN patients were given enalapril. The drugs were also examined for the action on systemic arterial pressure, renal function and intrarenal hemodynamics. Significantly decreased urinary excretion of protein occurred in DN patients on the treatment month 1, in CN subjects on month 3. In both groups ACE inhibitors produced marked hypotensive effect, did not affect renal function, noticeably improved intraglomerular hemodynamics. Hypotensive and antiproteinuria activity of the drugs were unrelated. The mechanism of antiproteinuria action of ACE inhibitors works via normalization of intrarenal hemodynamics. Systemic arterial hypertension seems to be an additional factor aggravating disturbances of intrarenal circulation and provoking proteinuria.