Belén Marrón

BACKGROUND: Timely referral, preparation and initiation of dialysis remain problematic issues. The purpose of this study is to analyse the effect of chronic renal disease care and education on the mode of dialysis start (planned vs non-planned) and on the modality of renal replacement therapy (RRT). METHODS: A total of 1504 patients from 35 hospitals started RRT in 2003. Out-patient, scheduled initiation of dialysis with a permanent vascular or peritoneal access was considered planned. RESULTS: About 46% of the patients started non-planned dialysis. Of all the patients, 75% had > or =3 months of nephrological follow-up, but nearly half were never educated on dialysis options. Haemodialysis (HD) occurred in 82% and peritoneal dialysis (PD) in 18%. Planned starts were associated (all P < 0.001) with many factors: younger age, longer renal and pre-dialysis follow-up, more education on RRT and general care, more medical visits, more PD (27 vs 8%), more follow-up by specific end-stage renal disease (ESRD) units, more permanent access and better biochemical status at the start of dialysis. Some global differences were found between patients: planned vs non-planned with > or =3 months of follow-up, vs non-planned <3 months follow-up or acute non-planned and <3 months of follow-up or acute patients. HD occurred in a similar rate (92%) in patients with non-planned start, no previous follow-up or who were never educated in dialysis modality options. CONCLUSION: Although a high prevalence of nephrologic care and follow-up was provided among incident patients in dialysis, nearly half the patients did not have a planned dialysis start nor dialysis modality education. Planned start was associated with better analytical and multidisciplinary status. PD was more prevalent in planned starts and when education was given. Specific ESRD units were more likely to provide an optimal care.

Persistent proteinuria is considered a deleterious prognostic factor in most progressive renal diseases. However, the mechanisms by which proteinuria induces renal damage remain undetermined. Since proximal tubular cells possess all the machinery to generate angiotensin II (Ang II), we approached the hypothesis that proteinuria could elicit the renal activation of the renin-angiotensin system in a model of intense proteinuria and interstitial nephritis induced by protein overload. After uninephrectomy (UNX), Wistar-Kyoto rats received daily injections of 1 g BSA or saline for 8 days. The mean peak of proteinuria was observed at the fourth day (538+/-89 versus 3+/-1 mg/24 h in UNX controls; n=12; P<0.05) and was increased during the whole study period (at the eighth day: 438+/-49 mg/24 h; n=12; P=NS). Morphological examination of the kidneys at the end of the study showed marked tubular lesions (atrophy, vacuolization, dilation, and casts), interstitial infiltration of mononuclear cells, and mesangial expansion. In relation to UNX control rats, renal cortex of BSA-overloaded rats showed an increment in the gene expression of angiotensinogen (2.4-fold) and angiotensin-converting enzyme (ACE) (2.1-fold), as well as a diminution in renin gene expression. No changes were observed in angiotensin type 1 (AT1) receptor mRNA expression in both groups of rats. By in situ reverse transcription-polymerase chain reaction and immunohistochemistry, ACE expression (gene and protein) was mainly localized in proximal and distal tubules and in the glomeruli. By immunohistochemistry, angiotensinogen was localized only in proximal tubules, and AT1 receptor was localized mainly in proximal and distal tubules. In the tubular brush border, an increase in ACE activity was also seen (5. 5+/-0.5 versus 3.1+/-0.7 U/mg protein x10(-4) in UNX control; n=7; P<0.05). Our results show that in the kidney of rats with intense proteinuria, ACE and angiotensinogen were upregulated, while gene expression of renin was inhibited and AT1 was unmodified. On the whole, these data suggest an increase in Ang II intrarenal generation. Since Ang II can elicit renal cell growth and matrix production through the activation of AT1 receptor, this peptide may be responsible for the tubulointerstitial lesions occurring in this model. These results suggest a novel mechanism by which proteinuria may participate in the progression of renal diseases.

BACKGROUND: Despite advances in predialysis care, morbidity and mortality remain high. OBJECTIVES: To analyze end-stage renal disease (ESRD) patient demographics and clinical data on education on dialysis treatment options, type of chronic renal replacement therapy (RRT), and effects of planned versus non-planned dialysis start. METHODS: 621 patients, from 24 Spanish hospitals, who started RRT in 2002. Peritoneal or vascular access at dialysis initiation was considered "planned." RESULTS: 304 (49%) patients were non-planned and half of them had prior nephrology follow-up. Of the patients with >3 months nephrology follow-up (76% of all), only half were educated on dialysis modalities. Dialysis education was associated with planned start in 73.4% versus 26% in non-educated patients (p < 0.05), shorter follow-up (55 vs 65 months, p = 0.033), more medical visits in the prior year (6.5 vs 4.4, *p < 0.001), more patients starting peritoneal dialysis (31% vs 8.3%*), and more specific follow-up by ESRD unit versus general nephrology care (63% vs 26%*). Non-planned start was associated with older age (63 vs 60.6 years, p = 0.06), fewer medical visits (4.6 vs 6.4*), less education about modality options, and greater use of hemodialysis (92% vs 75%*). Planned patients had better biochemical parameters at start of dialysis. CONCLUSION: Despite nephrology follow-up, half the patients did not have a planned dialysis start. Planned start was associated with better clinical status. More patients chose peritoneal dialysis when educated about dialysis modality options. ESRD-specific units were more likely to provide patient education.

OBJECTIVES: The rate of decline of residual renal function is slower in peritoneal dialysis (PD) than in hemodialysis. However, it is unclear which and whether either of the two techniques modifies the natural course of renal failure. We tested whether PD influences the natural course of the progression of chronic renal failure in humans. DESIGN: Retrospective review of clinical charts. SETTING: Tertiary-care center. PATIENTS: Fourteen patients were selected from the 36 patients that were treated with PD in our center from January 1997 to June 2000, applying the following criteria: predialysis follow-up longer than 12 months, renal creatinine clearance 20 mL/minute or more at the start of predialysis follow-up, follow-up while on PD longer than 6 months, and renal creatinine clearance above 0 mL/minute at the start of PD. MAIN OUTCOME MEASURE: Residual renal function calculated as renal creatinine clearance obtained from 24-hour urine samples. RESULTS: A lower mean rate of decline of residual renal function was observed during PD than during the predialysis period (-0.06 +/- 0.16 vs -0.94 +/- 0.74 mL/min/month, p < 0.0005). The rate of decline in renal creatinine clearance was faster in every patient during the predialysis period than during his or her time on PD. CONCLUSIONS: These preliminary data support the hypothesis that PD may contribute to the slowing of the natural progression of renal disease in humans, as it does in rodents. Prospective studies involving a larger number of patients are needed to settle the question.