In lung transplant recipients, the 1-month postoperative loss of GFR is an early marker for long-term renal prognosis. Pulmonary diagnosis appears to be a relevant predictor as well. These factors may guide further research and the development of preventive strategies.
ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This antihypertensive efficacy probably accounts for an important part of their long term renoprotective effects in patients with diabetic and non-diabetic renal disease. The renal mechanisms underlying the renal adverse effects of ACE inhibitors--intrarenal efferent vasodilation with a consequent fall in filtration pressure--are held to be involved in their renoprotective effects as well. The fall in filtration pressure presumably contributes to the antiproteinuric effect as well as to long term renoprotection. The former is suggested by the positive correlation between the fall in filtration fraction and the reduction in proteinuria found during ACE inhibition. The latter is suggested by the correlation between the (slight) reduction in glomerular filtration rate at onset of therapy and a more favourable course of renal function in the long term. Such a fall in filtration rate at the onset of ACE inhibitor treatment is reversible after withdrawal, and can be considered the trade-off for long term renal protection in patients with diabetic and nondiabetic chronic renal disease. In conditions in which glomerular filtration is critically dependent on angiotensin II-mediated efferent vascular tone (such as a post-stenotic kidney, or patients with heart failure and severe depletion of circulating volume), ACE inhibition can induce acute renal failure, which is reversible after withdrawal of the drug. Systemic and renal haemodynamic effects of ACE inhibition, both beneficial and adverse, are potentiated by sodium depletion. Consequently, sodium repletion contributes to the restoration of renal function in patients with ACE inhibitor-induced acute renal failure. Our the other hand, co-treatment with diuretics and sodium restriction can improve therapeutic efficacy in patients in whom the therapeutic response of blood pressure or proteinuria is insufficient. Patients at the greatest risk for renal adverse effects (those with heart failure, diabetes mellitus and/or chronic renal failure) also can expect the greatest benefit. Therefore, ACE inhibitors should not be withheld in these patients, but dosages should be carefully titrated, with monitoring of renal function and serum potassium levels.
Renal function impairment is common after solid organ transplantation, due to the nephrotoxicity of cyclosporine. Moreover, in patients with severe respiratory failure, renal function is often impaired. This renal function impairment may predispose patients to further renal function impairment after lung transplantation. Therefore, renal hemodynamics were measured in 44 patients before lung transplantation and 1, 6, 12, 18, 24, and 30 months after transplantation. After transplantation, a decline in renal function occurred, with a progressive fall in glomerular filtration rate (GFR) of 33 +/- 4% at 12 months and 42 +/- 9% at 30 months. Effective renal blood flow fell by 22 +/- 5% at 12 months and remained stable thereafter. Changes in effective renal plasma flow (ERPF) were less pronounced than those of effective renal blood flow, due to a fall in hematocrit after transplantation. Blood pressure and renal vascular resistance increased significantly, consistent with the effects of cyclosporine. Prior to transplantation, renal function impairment with intense renal vasoconstriction had been found in a subset of the patients. Remarkably, the decrease in renal function after transplantation was less pronounced in patients with renal function impairment prior to transplantation, as indicated by significant negative correlations between pretransplantation GFR and the percentage change in GFR after transplantation, and pretransplantation ERPF and the percentage change in ERPF after transplantation. This suggests that the net course of renal hemodynamics after lung transplantation is the result of the opposed effects of cyclosporine nephrotoxicity and the favorable effects of the normalization of respiratory status. In conclusion, after lung transplantation a decline in renal function occurs that is less pronounced in patients with renal function impairment and intense renal vasoconstriction prior to transplantation. Such a renal function impairment, therefore, should not be considered a contraindication to lung transplantation.
Agents that interfere with the renin-angiotensin system (RAS) reduce proteinuria and afford renal protection. The combination of different measures that serve maximization of RAS blockade is thought to improve the antiproteinuric efficacy. The feasibility and the efficacy of such a combination strategy were studied in nondiabetic patients with residual proteinuria during previous RAS blockade by individual antiproteinuric titration. P roteinuria nowadays is looked upon as an important and independent risk factor for progression of renal disease (1,2). Moreover, evidence from large clinical trials has become available, showing that reduction of proteinuria is important for long-term renoprotection (3,4). In addition, it has been noted that both residual proteinuria and the amount of antiproteinuric response are predictive for renal outcome in individual patients (5,6), indicating that residual proteinuria during therapy is a predictor of the individual renal prognosis. Accordingly, maximum reduction of proteinuria has been advocated as a treatment target for individual renal patients, in addition to control of BP (7-9). For optimal renoprotection, therefore, recent data suggest that treatment target for proteinuria should be Ͻ1 g/d and likely near zero (7,8).Intervention in the renin-angiotensin system (RAS) is currently the most effective strategy that combines renoprotection with proteinuria lowering. Roughly, the average antiproteinuric response of RAS blocking agents is 50%-both for angiotensin-converting enzyme inhibitors (ACEi) and for angiotensin II antagonists (AIIA) (10,11). There are several strategies to optimize the response, including dose titration of the RAS intervening agents (12), combining RAS blockade with lowsodium diet or a diuretic (13), and combining the different RAS blocking strategies (14). Indeed, ACEi plus AIIA renders more antiproteinuric effect and also more renoprotection (15). Although each of these measures is studied widely on the group level, until now, no individual data of maximal RAS blockade on proteinuria are available (9). Moreover, it is unknown whether it is possible, in a prospective manner, to obtain the target level of proteinuria Ͻ1 g/d by titrating these measures in individual patients. In the present study, our aim was to investigate the antiproteinuric potential of additional up-titration with an ACEi to maximal tolerated dose against a background of a maximal dosed AIIA combined with diuretic therapy in a sodium-restricted setting. Materials and Methods Patients and ProtocolPatients were selected from our renal outpatient clinic. All patients gave informed consent and fulfilled the inclusion criterion of a stable proteinuria Ͼ1 g/d and Ͻ10 g/d while they were still on their previous (nonimmune suppressive) antiproteinuric treatment. Moreover, only patients with BP Ͻ140/Ͻ90 mmHg, creatinine clearance Ն30 ml/min per 1.73 m 2 , and age between 18 and 70 yr were included. Patients with cardiovascular disease or diabetes were excluded, as well as frequent users of non...
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