[Progression of renal insufficiency in the pre-end-stage renal disease setting]. / Progresión de la insuficiencia renal en pacientes con enfermedad renal crónica avanzada.

The rate of decline of renal function (RDRF) in the pre-end stage renal disease setting (pre-ESRD) is highly variable. Several factors have been involved as potential modifiers of renal failure progression. This retrospective study attempts to establish which were the main determinants of the RDRF in pre-ESRD patients followed in the predialysis consult. The study group consisted of 230 patients with pre-ESRD not yet on dialysis who were referred to the predialysis consult from January 1998 to July 2002. The mean follow-up time per patient was 356 days. RDRF was assessed as delta of the average of creatinine and urea clearances (CrCl-UCl). Data obtained at time of referral to the predialysis consult were analyzed as potential predictors of the subsequent RDRF. These independent variables included: demographics, comorbid conditions, main hematological and biochemical data, antihypertensive and statin treatment, mean blood pressure, and CrCl-UCl at time of referral. The predictors of delta CrCl-UCl were determined by multiple linear regression analysis. The determinants of the survival without dialysis were established by the Cox regression hazard model, adjusted to renal function at time of referral. Mean CrCl-UCl at time of referral was 10.98 +/- 2.58 ml/min/1.73 m2, and mean delta CrCl-UCl was -0.37 +/- 0.46 ml/min/1.73 m2/month. Patients with diabetic nephropathy and chronic glomerulonephritis had the fastest RDRF, while patients with ischemic nephropathy and chronic interstitial nephritis had the slowest RDRF. Seventy-five patients (46%) required EPO therapy. The best determinants of delta CrCl-UCl were: the 24-hour proteinuria (p < 0.0001), and the hematocrit at time of referral (p = 0.0024). The best determinants of the survival rate without dialysis during the study period were: the proteinuria (in g/24 hours) (R 1, 16; p < 0.0001), the hematocrit at time of referral (OR: 0.88; p < 0.0001), the treatment with EPO (OR: 0.59; p = 0.02), and the diagnosis of diabetes mellitus (OR: 1.59; p = 0.01). In conclusion, apart from the rate of proteinuria, which could represent the best marker of the RDRF in chronic renal diseases, the development of anemia was associated with faster decline in renal function.

[Predictors of early death during dialysis]. / Predictores de la mortalidad precoz en diálisis.

The mortality among end-stage renal failure (ESRF) patients undergoing renal replacement therapy (RRT) remains high. An important proportion of these patients die shortly after the initiation of RRT. The present study aims to determine the best predictors for the early mortality in a group of 140 ESRF patients who initiated RRT between october 96 and december 99. The mean age of the study group was 61 +/- 13 years, and the mean follow-up time was 20 +/- 12 months. Diabetic nephropathy was the most prevalent etiology of renal failure (30%). The following data, collected immediately before the initiation of RRT, were included as independent variables: demographic and clinical characteristics, including the nutritional status established by the Subjective Global Assessment (SGA), follow-up time in the predialysis clinic (less or longer than 3 months), EPO therapy, vascular access, renal function (creatinine and urea clearances, and Kt/V urea), hematological and biochemical data including serum albumin, bicarbonate, transferrin, PTH and C-Reactive protein, as well as the protein catabolic rate and the percent of lean body mass normalized for ideal body weight, calculated from the 24 h total urine excretion of nitrogen and creatinine. The Cox proportional hazard regression model, stratified for an age over or less than 65 year, was utilized to determine the best predictors for the mortality during the study period. Sixty percent of patients had at least one comorbid condition, and 35% had cardiovascular diseases. Mild-moderate or severe malnutrition was observed in 48% of patients. The creatinine clearance and Kt/V urea before the initiation of RRT were: 9.50 +/- 2.64 ml/min/1.73 m2 and 1.47 +/- 0.44, respectively. Forty-one patients died during the study period (annual death rate: 17%). The best predictor of mortality was the nutritional status assessed by the SGA (OR: 2.32, IC 95% 1.54-3.48, p < 0.0001). In a second analysis in which the SGA was removed from the model, the previous history of cardiovascular diseases (OR: 2.07, CI 95%: 1.06-4.06, p = 0.032), and the percent of lean body mass/ideal weight (OR: 0.96; IC 95%: 0.93-0.99; p = 0.042), proved to be the best predictor of mortality. In conclusion, nutritional indices prior to the initiation of RRT, and the previous history of cardiovascular diseases were the best predictors of the early mortality in this unselected population on dialysis. Because nutritional status appeared to be a marker of the severity of the comorbid conditions, a better control of the number and severity of these comorbid conditions may be the best way for reducing the mortality in patients on RRT.

Sympathetic skin response in hemodialysis patients: correlation with nerve conduction studies and adequacy of dialysis.

A sympathetic skin response (SSR) test was performed in diabetic and nondiabetic patients undergoing regular hemodialysis and the results correlated with nerve conduction studies (NCS): sensory conduction velocity (SCV) and motor conduction velocity (MCV). Comparisons were made between diabetic and nondiabetic patients and between cuprophane and polyacrylonitrile membrane dialyzed patients. Six nondiabetic uremic patients (30%) and all diabetic patients had no SSR. Eight nondiabetic uremic patients (40%) had a mildly impaired response. Nondiabetic patients with a normal response were younger (31.1+/-16.4 years) than the patients with abnormal SSR, whether mildly impaired response (58.3+/-20.3 years; p<0.05, Anova) or absent response (65.3+/-13.8 years; p<0.01, Anova). SCV, MCV, and SSR values were reduced (p<0.01) in uremic patients with respect to normal subjects. Severity and frequencies of sensory NCS abnormalities in nondiabetic patients were: normal 20%, mildly impaired 75%, and severely impaired 5%. Severity and frequencies of motor conduction abnormalities were: normal 80%, mildly impaired 20%, severely impaired 0%. The SSR abnormality incidence in patients with a normal NCS was similar to that in patients with either mildly or severely impaired NCS (chi-square test). There was a positive linear correlation between the SSR amplitude and SCV (r = 0.52, p<0.01) and MCV (r = 0.49, p<0.01). The SSR latency was also significantly related to SCV (r = 0.66, p<0.01) and MCV (r = 0.61, p<0.01). A significant negative correlation was found between age and SSR parameters, amplitude (r = -0.56, p<0.01) and latency (r = -0.66, p<0.01). No correlation was found between duration of hemodialysis or Kt/V and SSR. No differences were found in SSR, NCS, or Kt/V values between cuprophane membrane and polyacrylonitrile membrane dialyzed patients (Student's t test). The relationship between NCS and SSR in uremic patients was confirmed. Old age and diabetes mellitus, but not the dialysis membrane used, were confirmed as synergistic factors of neuropathic impairment. It appeared that SSR is more sensitive than NCS in detecting polyneuropathy in uremic patients on hemodialysis.

Metabolic acidosis in advanced renal failure: differences between diabetic and nondiabetic patients.

Metabolic acidosis is almost invariably a consequence of advanced renal failure, although its severity can vary widely. To evaluate the determinants of the severity of metabolic acidosis, with special interest in determining if there is any difference in the prevalence and severity of metabolic acidosis between patients with and without diabetes, 113 predialysis patients with renal failure were studied. Criteria for inclusion onto the study were: creatinine clearance (Ccr)/1.73 m2 less than 30 mL/min, no alkali therapy within the previous 30 days, and the absence of respiratory diseases. Forty-eight patients had diabetes (33 patients with diabetic nephropathy). The following data were analyzed: demographics; cause of renal failure; hematocrit; serum urea, creatinine, uric acid, albumin, glucose, hemoglobin A1c, bicarbonate, sodium, potassium, chloride, calcium, phosphorus, and alkaline phosphatase levels; anion gap; urinary protein excretion; Ccr/1.73 m2; half of the sum of creatinine and urea clearances (Ccr-Cu); protein-equivalent nitrogen appearance (PNA); and whether the patients received diuretics (75 patients), angiotensin-converting enzyme inhibitors (54 patients), and/or calcium channel blockers (55 patients). After the exclusion of eight patients because of hypochloremia (three patients with and five patients without diabetes), mean serum bicarbonate levels were significantly greater in patients with diabetes than in the rest of the patients (20.7 +/- 2.3 v 18.2 +/- 2. 3 mmol/L; P = 0.0001). The mean anion gap (mmol/L) was also significantly less in patients with than without diabetes (19.70 +/- 3.65 v 22.35 +/- 3.64; P = 0.003). Eleven of 105 patients had serum bicarbonate levels of 23 mmol/L or greater (9 patients with and 2 patients without diabetes). Pure elevated anion gap followed by mixed (high anion gap and hyperchloremia) were the most common types of metabolic acidosis observed in both groups. There were no differences in PNA, diuretic treatment, or vomiting history between patients with and without diabetes. By multiple logistic regression analysis, the best determinants for a serum bicarbonate level greater than 19 mmol/L were: the diagnosis of diabetic nephropathy (odds ratio, 0.107; P = 0.0002), Ccr-Cu (odds ratio, 0.824; P = 0. 014), and age (odds ratio, 0.966; P = 0.046). In conclusion, patients with diabetes with advanced renal failure showed a less severe metabolic acidosis, which cannot be explained by gastrointestinal hydrogen ion losses, drugs, or reduced protein catabolic rate. Patients with diabetes may have a more efficient extrarenal generation of bicarbonate than end-stage renal failure patients without diabetes.

Hemodialysis with cuprophane or polysulfone: effects on uremic polyneuropathy.

A longitudinal study was performed of 11 patients on hemodialysis (HD) who where changed from cuprophane (CU) to polysulfone (PSF) membranes. Delivered Kt/V was approximately 1.1 throughout the study period. Motor conduction velocities (MCV) and sensory conduction velocities (SCV) were measured predialysis and postdialysis while the patients were still on CU membranes, 1 month after changing to PSF, and 12 months after changing to PSF. There was no change in predialysis MCV or SCV. For example, predialysis MCV with CU (43.6 +/- 6.2) was still 43.6 +/- 4.8 m/s after 1 year of PSF dialysis (P = NS). Similarly, predialysis SCV with CU (45.1 +/- 4.6 m/s) was not increased after 1 year of PSF dialysis (42.0 +/- 3.6 m/s). However, the predialysis versus postdialysis comparisons did show a difference between CU and PSF for SCV. PSF dialysis increases SCV by 3.0 +/- 3.8, whereas with CU dialysis the increase in SCV (0.7 +/- 2.4) was not significant (delta SCV-CU v delta SCV-PSF, P < 0.05). Acutely, dialysis with both CU and PSF increased MCV by the same amount (CU, 1.5 +/- 2.1; PSF, 2.8 +/- 3.5; delta MCV-CU, P < 0.05; delta MCV-CU v delta MCV-PSF, P = NS). The results suggest that dialysis with PSF membranes acutely improved SCV more than dialysis with CU membranes. However, changing to PSF does not improve predialysis SCV values. Dialysis with both membranes improves MCV to the same extent.

Calcium acetate versus calcium carbonate as phosphate binders in hemodialysis patients.

We conducted a randomized unblinded parallel clinical trial to compare the effectiveness, side effects and tolerance between calcium acetate (CA) and calcium carbonate (CC) in 80 stable chronic hemodialysis patients selected on the basis of their acceptable control of serum phosphorus (P) levels with aluminum hydroxide (AH). All patients were dialyzed against the same calcium dialyzate (1.62 mmol/l). The serum analytical tests included: calcium corrected to total protein, P, PTH (intact molecule) and bicarbonate. The study was divided into the following periods: P0: baseline measurements; P1: washout (withdrawal of AH for 15 days); P2: random allocation to CA and CC treatment at doses equivalent to 75 mEq of elemental calcium, stratified according to previous doses of AH (2 months); P3: adjustment of doses until control P (2 months). CA was poorly tolerated in 7 patients and CC in 2 (NS). The changes in serum P levels between P0 and P2 periods were lower in the CA group (1.73 +/- 0.25 vs. 1.80 +/- 0.50 mmol/l; p = 0.26) than in the CC group (1.77 +/- 0.35 vs. 1.93 +/- 0.48 mmol/l; p = 0.03, paired t test). Serum calcium was hardly modified by CA (2.42 +/- 0.20 vs. 2.47 +/- 0.17 mmol/l; NS) while in the CC group, it rose significantly (2.40 +/- 0.12 vs. 2.55 +/- 0.22 mmol/l; p = 0.0004). There were no differences in the control of PTH or bicarbonate.(ABSTRACT TRUNCATED AT 250 WORDS)