Alessandro G. Bellucci

Renal Vascular Disease Causing End-Stage Renal Disease, Incidence, Clinical Correlates, and Outcomes: A 20-Year Clinical Experience

In the United States, the incidence of end-stage renal disease to hypertension has increased sharply over the last 8 years, especially in elderly white dialysis patients who demonstrate very poor survival rates. The 5-year survival rates were near 20% for patients 65 to 74 years old and 9% for those > or = 75 years of age. Our program experienced a sharp increase in cases of end-stage renal disease due to renal vascular disease after 1982. Renal vascular disease was characterized clinically in 83 of 683 dialysis patients either by angiography or asymmetric kidney size in patients with evidence of systemic atherosclerosis, hypertension, insignificant proteinuria, and a benign urinary sediment. The median age was 70 years, with 84% of the patients being older than 61 years. These patients had 56% 2-year, 18% 5-year, and 5% 10-year survival rates, which are quite similar to the 1992 US Renal Data System data. Patients with renal vascular disease have a significantly worse prognosis than other diagnostic groups, most likely due to their older age, underlying vascular disease, and coronary artery disease. We feel that a significant number of elderly white hypertensive patients described in the 1992 US Renal Data Service report have renal vascular disease as a cause of end-stage renal disease, highlighting the need to establish correct renal diagnoses. Hypertension should not be the end-stage renal disease diagnosis in elderly white hypertensive patients if clinical criteria suggest a diagnosis of renal vascular disease.

Comparison of methods for measuring albumin in peritoneal dialysis and hemodialysis patients

Serum albumin levels have been used extensively as an indicator of morbidity in patients with end-stage renal disease. Recent evidence suggests that albumin levels vary considerably in hemodialysis patients depending on the laboratory method used, but formulas for comparing albumin values by different methods have not been developed. We prospectively evaluated the effects of measuring albumin by three different methods on paired plasma and serum from 23 patients on continuous ambulatory peritoneal dialysis (CAPD) and 53 patients on chronic maintenance hemodialysis. Plasma and serum gave virtually identical results independent of method used. In CAPD patients, bromcresol green and nephelometry gave nearly identical albumin measurements through the entire range of plasma levels. In contrast, bromcresol purple gave values that were 9.9 percent +/- 1.3 percent lower (P < 0.05). Hemodialysis patients showed a similar pattern with close agreement between bromcresol green and nephelometry, but bromcresol purple gave lower albumin levels by 19.1 percent +/- 1.2 percent (P < 0.05). The discrepancy in albumin in CAPD patients was significantly less than in the hemodialysis patients (P < 0.05), suggesting that there were fewer interfering substances in the blood of CAPD patients than in hemodialysis patients. Linear regression analysis was used to develop simple formulas for comparing albumin values obtained by the different methods in CAPD and hemodialysis patients. These studies show that values for albumin in blood vary significantly by method of analysis in CAPD and hemodialysis patients. By the use of these formulas, it becomes possible to compare albumin values between centers using different methods for the purpose of quality management.

PLASMA ANGIOTENSINS IN ANEPHRIC HUMANS : EVIDENCE FOR AN EXTRARENAL ANGIOTENSIN SYSTEM

The recent identification of messenger RNAs encoding renin and angiotensinogen in nonrenal tissues raises the possibility that angiotensins (Ang) may be formed extrarenally and released into the plasma. The aim of this investigation was to test the hypothesis that plasma angiotensins may originate from extrarenal sites. Twenty-five patients with chronic renal failure (six surgically anephric and 19 with kidneys in situ) were studied prior to and after a standard hemodialysis treatment. Angiotensins were measured by extraction. high-pressure liquid chromatography (HPLC) separation, and radioimmunoassays. In patients with kidneys present, plasma renin activity (PRA) was 3.1 ± 0.7 ng Ang I/ml/h. Ang I, Ang II. and Ang III levels were 70.6 ± 9.0. 44.0 ± 9.8, and 20.2 ± 3.6 pg/ml, respectively. In all six anephric patients PRA was undetectable ±0.1 ng Ang I/ml/h). Ang I and Ang II were detected in four anephric patients, and Ang III was detected in three anephric patients (Ang I, (10.4 ± 5.2; Ang II, 2.6 ± 1.2; Ang III. 2.7 ± 1.5 pg/ml, n = 6). At the completion of dialysis treatments, which reduced body weight by 2.5 ± 0.2 kg in patients with kidneys and by 2.1 ± 0.3 kg in anephric patients, there were no significant changes in PRA or plasma angiotensins in either group. Reduction in body water by hemodialysis did not increase the concentration of angiotensins in plasma. We conclude that there is a small but definite component of plasma angiotensin that is produced by nonrenal mechanisms and that is not stimulated by volume depletion.

Metoclopramide decreases renal plasma flow

Intravenous dopamine has been shown to increase renal plasma flow in man. The role of endogenous dopamine in the maintenance of renal plasma flow has not been described. We speculated that if endogenous dopamine activity is important in the maintenance of renal plasma flow, then high doses of a potent dopamine blocking drug such as metoclopramide would decrease renal flow. To test this hypothesis, we measured renal plasma flow using a single‐injection technique with 131I‐labeled orthoiodohippurate. Measurements were made before and after the administration of high doses of metoclopramide (1 to 2.5 mg/kg) to 20 patients receiving metoclopramide as an antiemetic before chemotherapy. Seven control subjects underwent sequential measurements of renal plasma flow without intervening metoclopramide dosing. Mean (±SD) renal plasma flow did not change in the control population (from 441 ± 198 to 437 ± 117 ml/min), but declined significantly in the patients who received metoclopramide (443 ± 115 ml/min before metoclopramide and 387 ± 137 ml/min after metoclopramide; P < 0.001). In 25% of our study population the decline in renal plasma flow was >20% below baseline levels. The magnitude of the effect did not appear to correlate with the pretreatment creatinine clearance, age, or sex of the patients. We conclude that high doses of metoclopramide decrease renal plasma flow in man. These data suggest a role for dopamine in the maintenance of renal plasma flow in patients receiving intravenous hydration. Changes of the magnitude we observed may well be of clinical importance. These findings therefore also suggest the possibility of metoclopramide potentiation of cisplatin nephrotoxicity.