Inhibitors of the renin-angiotensin system reduce the rate of GFR decline and end-stage renal disease in patients with severe renal insufficiency.

Drugs that inhibit the renin-angiotensin system (RAS) are of proven benefit in the treatment of hypertension, congestive heart failure, or acute myocardial infarction. In the last decade, several clinical trials have shown that RAS inhibitors also offer significant renoprotection in both diabetic and non-diabetic nephropathy. However, patients with advanced renal insufficiency did not take part in these trials because of the risk of acute renal failure (ARF) and hyperkalemia, and, for the same reason, most physicians do not offer these drugs to patients with impaired renal function. Recently, a post-hoc analysis of the Ramipril Efficacy In Nephropathy (REIN) study which included patients with severe renal insufficiency, showed that RAS inhibition slows glomerular filtration rate (GFR) decline over time and progression to end-stage renal disease (ESRD) in a safe way in patients quite close to ESRD (basal GFR, 10 to 30 ml/min/1.73m2). These beneficial effects have also been shown in the Reduction of Endpoints in NIDDM with the All Antagonist Losartan (RENAAL) study, in patients with type 2 diabetes mellitus, clinical proteinuria, and renal insufficiency, where RAS inhibition therapy significantly reduced the risk of ESRD once doubling of baseline serum creatinine levels had been achieved as compared to non-RAS anti-hypertensive treatment. Thus, these data suggest that RAS inhibition therapy should be given to all patients with proteinuric chronic nephropathy, independently of the level of renal function.

Maintenance hemodialysis and circulating ionized magnesium.

BACKGROUND: Circulating magnesium exists in the bound and in the free ionized form, that is biologically active. In kidney disease the relationship between ionized and total circulating magnesium is often altered. Little information is available on the influence of hemodialysis on the relationship between ionized and total circulating magnesium in end-stage kidney disease. METHODS: Plasma total and ionized magnesium and the plasma ionized magnesium fraction were assessed before and after hemodialysis (dialysate magnesium content 0.75 mmol/l) in 46 patients with end-stage kidney disease and in a control group of 25 healthy subjects. RESULTS: In patients plasma total (from 1.19 [1.05-1.33] to 1.10 [1.02-1.16] mmol/l; median and interquartile range) and ionized (from 0.71 [0.66-0.78] to 0.65 [0.63-0.69] mmol/l) magnesium significantly decreased during dialysis (control subjects: 0.82 [0.80-0.92], respectively, 0.57 [0.54-0.59] mmol/l). The plasma ionized magnesium fraction was significantly lower in patients both before (0.61 [0.58-0.64)] and after (0.60 [0.56-0.62]) hemodialysis than in controls (0.68 [0.65-0.70]). CONCLUSIONS: The study demonstrates a tendency towards a reduced circulating ionized magnesium fraction in end-stage kidney disease that is not corrected by hemodialysis.