A survival analysis was applied to 1,453 patients treated between 1972 and 1978 in 33 French dialysis centers and prospectively followed up in the computerized Diaphane Dialysis Registry. 198 deaths (overall mortality = OM) were registered, of which 87 (43%) were secondary to cardiovascular complications (cardiovascular mortality = CVM). Risk factors for OM and CVM (p values < 0.05) were age, male sex, nephroangiosclerosis or diabetic nephropathy as the primary renal disease, elevated systolic and diastolic blood pressure and two weekly dialysis rather than three. In contrast with the results observed for the general population, a high body mass index and elevated cholesterol, triglycerides and uric acid were not found to be associated with significantly increased CVM or OM. On the contrary, low body mass index ( < 20 kg/m²), low cholesterol ( < 4.5 mmol/l) and low mean predialysis blood urea ( < 4.6 mmol/l) were associated with increased OM and CVM, and more especially with high stroke mortality. Results for urea but not for cholesterol remain significant after adjustment for age, sex, weekly dialysis schedule and body mass index. They suggest that, in addition to elevated blood pressure, a poor nutritional state and/or low protein intake may be important factors for explaining the high cardiovascular mortality, particularly for strokes, observed in dialyzed patients.

Epo significantly enhanced the rate of recovery from acute renal failure induced by cisplatin. PCNA staining indicated that Epo might act directly via stimulation of tubular cell regeneration.

The European Survey of Anaemia Management 2003 (ESAM 2003) was a 1 day randomized survey conducted to assess anaemia management in dialysis patients 4 years after the introduction of the European Best Practice Guidelines. The survey included 8100 patients from 11 European countries and Israel. Overall, haemoglobin (Hb) levels > or =11.0 g/dl, as recommended by the guidelines, were achieved in 66% of patients. Only 48% of patients had adequate iron status, with transferrin saturation values missing for 27% and functional or absolute iron deficiency reported for 17 and 9%, respectively. In order to identify factors affecting epoetin dose and Hb levels, the countries were divided into two groups based on the percentage of patients with Hb levels > or =11.0 g/dl (>70% in group 1 and 60-70% in group 2). The most probable causes for better management in group 1 were administration of higher epoetin doses and better monitoring and management of iron status. In patients with Hb <11.0 g/dl, mean epoetin-alpha/beta doses were significantly lower for subcutaneous than intravenous (i.v.) administration, whereas mean doses were similar for both routes in patients with Hb > or =11.0 g/dl. When standardized for Hb levels, the dose ratio of i.v. epoetin-alpha/beta to i.v. darbepoetin alfa was 176:1 (95% confidence interval, 166:1-189:1). Limited comparisons between the eight countries that participated in ESAM 2003 and the original ESAM revealed that many patients still have haemoglobin levels below the current recommendations despite significant improvements in management of renal anaemia over the last 5 years.

These studies were designed to test the hypothesis that adenosine and calcium are important in mediating radiocontrast-media-associated reduction in renal blood flow (RBF) in the dog. Intravenous verapamil (V) and diltiazem (DTZ) infusion significantly attenuated the magnitude of the vasoconstrictor response observed after each intrarenal contrast media (CM) injection. (First injection: -47 ± 8% control vs. -14 ± 3% V, p < 0.03; -38 ± 4% control vs. -19 ± 3% DTZ, p < 0.02. Second injection: -33 ± 6% control vs. -12 ± 1 % V, p < 0.03; -32 ± 5% control vs. -17 ± 2% DTZ, p < 0.03. Third injection: -32 ± 6% control vs. -11 ± 5% V, p < 0.03; -38 ± 5% control vs. -10 ± 5% DTZ, p < 0.02.) Furthermore, V and DTZ almost completely abolished the increase in renal vascular resistance (RVR) induced by each CM administration. Theophylline also significantly attenuated the magnitude of the vasoconstrictor response observed after CM injection (first injection: -31 ± 3% control vs. -12 ± 3% theophylline, p < 0.05; second injection: -26 ± 3% control vs. -12 ± 3% theophylline, p < 0.03). Similarly, theophylline blunted the increase in RVR induced by CM injection. In addition, theophylline inhibited exogenous adenosine-induced decrease in RBF (-61 ± 10% and -26 ± 1 % decrease in RBF without and with theophylline, respectively). In contrast, dipyridamole significantly enhanced the vasoconstriction induced by CM (first injection: 25 ± 3% control vs. 49 ± 4% dipyridamole; second injection: 31 ± 3% control vs. 48 ± 4% dipyridamole p < 0.05). The effect of dipyridamole was abolished by simultaneous theophylline infusion. The vasoconstriction-induced CM was also enhanced during an ischemia (41 ± 11 vs. 28 ± 9%) induced by a reduction in renal perfusion pressure with an aortic clamp. Our data support the contention that endogenous adenosine and calcium action are essential for the effect of CM on RBF. We suggest that infusion of hypertonic radiocontrast agents result in an increase in sodium transport as has been documented with infusion of hypertonic saline with subsequent intrarenal generation of adenosine and activation of calcium-dependent vasoconstriction. Furthermore, our results in the ischemic kidney may explain why CM-induced acute renal failure occurs mainly in patients with preexisting renal failure.

The objectives of this study were first to develop a reproducible and reversible model of acute renal failure following contrast medium infusion in the rat; second to use that method to compare the nephrotoxicity of low- and high-osmolar contrast agents. Contrast media or saline were perfused in the aorta while a clamp was applied on the aorta just above the renal artery. Three minutes of renal ischemia with or without infusion of isotonic saline induced no change in serum creatinine and a slight and transient decrease in creatinine clearance at 24 h. Urinary N-acetyl glucosamidase (NAG) excretion was not modified in this control group. All 17 kidneys which were examined were normal. 2,100 mosm/kg hypertonic saline induced a significant increase in serum creatinine and a significant decrease in creatinine clearance (from 1.8 ± 0.1 to 0.8 ± 0.1 and 1.0 ± 0.2 ml/min at 24 and 48 h, respectively). Urinary NAG excretion increased from 23 ± 18 to 48 ± 20 and 8 ± 4 umol hrVmmol creatinine at 24 and 48 h, respectively (p < 0.05). Histologic analysis of 5 kidneys revealed acute tubular necrosis (n = 3) and no histologic abnormalities (n = 2). Diatrizoate induced an acute and reversible renal failure. Creatinine clearance decreased from 1.6 ± 0.1 to 0.4 ± 0.1 and 0.8 ± 0.1 ml/min at 24 and 48 h, respectively (p < 0.01). Urinary NAG excretion increased also significantly from 43 ± 9 to 352 ± 79 and 64 ± 23 umol h^_1/mmol creatinine at 24 and 48 h, respectively. Histologic examination of 7 kidneys revealed acute tubular necrosis (n = 4), tubular cytoplasmic vacuolization (n = 2), and no histologic abnormalities (n = 1). Ioxaglate and iopamidol induced no change in serum creatinine and a slight decrease in creatinine clearance comparable to that observed in the control group. Ioxaglate and iopamidol induced a significant increase in urinary NAG excretion at 24 h (ioxaglate: 31 ± 6 to 147 ± 31; iopamidol: 55 ± 20 to 123 ± 31 umol h^_1/mmol creatinine) which was completely reversible at 48 h (ioxaglate: 31 ± 9; iopamidol: 41 ± 8). Histological analysis of 8 kidneys exposed to ioxaglate revealed tubular cytoplasmic vacuolisation (n = 7) and no histologic abnormalities (n = 1). Histological analysis of 10 kidneys exposed to iopamidol revealed tubular cytoplasmic vacuolization (n = 8) and no histologic abnormalities (n = 2). We have described a reproducible and reversible model of contrast-medium-induced acute renal failure in the rat. In this model, ionic and nonionic low-osmolar contrast agents are less nephrotoxic than high-osmolar contrast agents.