title: Hypertension and progression of renal insufficiency.
abstract: Besides defining the appropriate doses of frusemide in uraemic patients, A. Heidland's contribution to the treatment of hypertension in chronic renal failure consisted in the following demonstrations: (1) In patients on chronic haemodialysis, calcium antagonists have a beneficial effect on their glucose intolerance and decreased plasma levels of 25OH vitamin D while their effect on blood lipids is neutral. (2) In 5/6 nephrectomized rats, captopril, verapamil, and metoprolol have the same protective effect on their GFR and tubular secretion of protons, at equal blood-pressure-lowering effect. (3) In rats with streptozotocin-induced diabetes, atrial natriuretic peptide does not play a role in their hyperfiltration. (4) Severe retinopathy is observed in patients with uraemic nephropathies at a much smaller elevation of their blood pressure than in patients with essential hypertension. This article reviews the following points: (1) The role of hypertension in the loss of renal function is convincingly demonstrated only in a few experimental models, and in man only in malignant hypertension and diabetic nephropathy but not in essential hypertension nor in non-diabetic nephropathy. However, preliminary results suggests that antihypertensive treatment may retard the progression of renal disease in normotensive patients (DBP <90 mmHg) with either microalbuminuric diabetes and normal renal function or non-diabetic uraemic nephropathy. (2) Only the ACE inhibitors have been proved to have a specific renal protective effect, independent of their diurnal blood-pressure-lowering effect, both in diabetic nephropathy and in non-diabetic uraemic nephropathy.
authors.affiliation: Service de Néphrologie-Médecine Interne du CHU d'Amiens, France.
authors.forename: A
authors.initials: A
authors.lastname: Fournier
authors.forename: N
authors.initials: N
authors.lastname: el Esper
authors.forename: R
authors.initials: R
authors.lastname: Makdassi
authors.forename: P
authors.initials: P
authors.lastname: Hué
authors.forename: P F
authors.initials: PF
authors.lastname: Westeel
authors.forename: J M
authors.initials: JM
authors.lastname: Achard
authors.forename: J D
authors.initials: JD
authors.lastname: Lalau
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure; D002121:Calcium Channel Blockers / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy; D007668:Kidney / Q000187:drug effects; D007674:Kidney Diseases / Q000150:complications / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000503:physiopathology*; D051381:Rats
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers