Dual renin-angiotensin system blockade: in patients with single functioning kidney and proteinuria.

AIM: Dual blockade of renin-angiotensin system (RAS) has increased antiproteinuric effects and it has been increasingly used on patients with proteinuria, but could have secondary effects when this kind of treatment is administered to patients with single functioning kidney. The aim of this study has been to assess the efficacy and safety of dual blockade of RAS in this group of patients. DESIGN AND METHODS: Sixteen patients with a single functioning kidney have been treated in our unit with dual RAS blockade due to proteinuria higher than 1 g/24 h. Mean age was 54.7+/-12.1 years, they were 12 males and 4 females. Analytical data of six months visit and last follow up visit have been retrospectively registered. Several different angiotensin conversor enzyme (ACE) inhibitors and angiotensin receptor blocking (ARB) drugs were used at the maximal dose tolerated by the patient. RESULTS: A small but not significant reduction of SBP and DBP were was observed throughout the study. Mean K+ increase in the second visit (from 4.65+/-0.67 to 5.01+/-1.02 mmol/l, not significant). There were no changes neither in plasmatic creatinine (baseline 1.86+/-0.67, 6 months 1.96+/-0.85) nor in creatinine clearance (baseline 65.2+/-26.9, 6 months 61.6+/-23.8 ml/min). Proteinuria was not reduced by dual RAS blockade (baseline 4.26+/-0.24, 6 months 4.25+/-0.39). CONCLUSIONS: Dual RAS blockade seems to be safe but unhelpful in renal patients with proteinuria associated to single functioning kidney.

Papel de la cistatina C en la valoración de la función renal y su relación con el riesgo cardiovascular / Role of cystatin C in the assessment of renal function and its relationship with cardiovascular risk

Actualmente no hay consenso sobre la forma ideal de medir la función renal. Durante décadas se ha utilizado la creatinina plasmática como el principal método de medición de la función renal, pero es una medición grosera y con frecuentes resultados erróneos. Para salvar estos obstáculos se han introducido fórmulas para calcular el aclaramiento de creatinina (fórmula de Cockroft-Gault) o el filtrado glomerular (ecuación del estudio Modification of Diet in Renal Disease). Por otra parte, se ha propuesto la cistatina C como un buen marcador de la función renal. Desgraciadamente, y a pesar del entusiasmo despertado, la cistatina C sólo parece mejorar ligeramente el poder predictor de la creatinina. La necesidad de esta medición ha ganado en importancia tras comprobarse que incluso pacientes con leves reducciones de la función renal presentan una morbilidad y mortalidad cardiovasculares elevadas. En este sentido la cistatina C podría ser un marcador de importancia pronóstica de la aparición de acontecimientos cardiovasculares independientemente de la función renal

Currently there is no agreement on the ideal way to measure renal function. Plasma creatinine has been used for decades as the principal method of renal function measurement. However, it is a rude measurement with frequent erroneous results. To overcome these obstacles, formulas have been introduced to calculate creatinine clearance (Cockroft-Gault formula) or glomerular filtration rate (equation of the Modification of Diet in Renal Disease Study). On the other hand, cystatin C has been proposed as a good marker of renal function. Unfortunately, and in spite of the enthusiasm provoked, cystatin C only seems to slightly improve the predictive power of creatinine. The need for this measurement has gained importance after verifying that even patients with mild reductions in renal function have elevated cardiovascular morbidity and mortality. In this sense, cystatin C could be a marker of prognostic importance of the appearance of cardiovascular events independently of the renal function

Sobredosis de ciamida cálcica (carbimida): descripción de un caso y revisión bibliográfica / Carbimide overdosage: description of a case and review of the literature

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[Obesity and mortality in advanced chronic renal failure patients]. / Obesidad y mortalidad en pacientes con insuficiencia renal avanzada.

A protective effect of obesity on the mortality of end-stage renal failure patients has been observed in several studies. Most of these studies have been based on prevalent dialysis population. The aim of the present study was to evaluate if obesity has beneficial effects on the survival of advanced chronic renal failure patients. The study group consisted of 376 patients (mean age 63 +/- 15 years) with advanced chronic renal failure not yet on dialysis. Obesity was defined as a body mass index (BMI) > or = 30 kg/m2. Grade of comorbidity was quantified by the method devised by Davies. Survival was analyzed as time from the referral to the predialysis outpatient clinic to patient death, censoring from contributing additional survival data to the analysis following transplantation. Kaplan-Meier analysis was used to test survival differences according to quartiles of BMI, and between obese and nonobese patients. Further analysis were performed, stratifying survival curves by comorbid scores, lean body mass, age, and sex. Cox proportional hazard regression models were used to investigate the best determinants of mortality, and the role of obesity adjusted for other covariates. Median survival time was 1,453 days. During the follow-up time, 158 patients (42%) died. Survival differences among quartiles of BMI were statistically significant (Breslow = 10.7, p = 0.017). Patients within the lowest and the highest quartiles of BMI had higher mortality than the rest of patients. Survival curves between obese and non-obese patients did not differ significantly. However, when patients without comorbidity were studied apart, those with obesity showed worse survival than the rest of patients (log-rank = 7.42, p = 0.0064). Since the effect of obesity on mortality did not follow a proportional hazard pattern throughout the study period, multivariable analysis for mortality was stratified by 18 months intervals. The variables which fitted the best model were: age (Hazard Ratio: 1.04), comorbid score (HR: 2.17), serum albumin (HR: 0.62), GFR at the study entry (HR: 0.91), male gender (HR: 1.48), and obesity (HR: 1.51). In conclusion, obesity had no survival benefit in patients with advanced chronic renal failure. Obesity had a noteworthy impact on early mortality of advanced chronic kidney disease patients without comorbidities.

Effects of oral phosphorus supplementation on mineral metabolism of renal transplant recipients.

BACKGROUND: Persistent hyperparathyroidism (HPT) is frequently observed in kidney transplant recipients. Hypophosphataemia is a common biochemical consequence of HPT. Theoretically, oral phosphorus administration may induce negative effects on the control of HPT, though this point has never been demonstrated in kidney-transplant recipients. This study was designed to evaluate the effects of oral phosphorus supplementation on the mineral metabolism of successful kidney transplant recipients. METHODS: Thirty-two kidney transplant recipients with serum creatinine < 2 mg/dl and serum phosphate levels <3.5 mg/dl were included in the study. After a washout period in which oral phosphorus supplementation was discontinued, the following parameters were determined (F0 period): serum calcium, phosphate, alkaline phosphatase, uric acid, bicarbonate, PTH, 1,25-dihydroxyvitamin D3 (1,25 (OH)(2)D) and 25-hydroxyvitamin D3 (25OHD). Creatinine clearance, calcium, and phosphate excretion were determined from a 24-h urine sample. The same determinations were repeated (F1 period) after all patients received 1.5 g of oral phosphorus for 15 days. For data analysis, patients were divided into two subgroups (optimal and suboptimal) according to allograft function (Ccr>or < 70 ml/min/1.73 m2). RESULTS: In the F0 period, only nine of 32 patients had PTH levels within the normal range (<65 pg/ml). The mean concentrations of PTH, 1,25(OH)(2)D and 25OHD were 132+/-97pg/ml, 40.5+16pg/ml and 12.5+/-8.2 ng/ml respectively. Phosphorus supplementation led to significant reductions in serum calcium and 1,25(OH)(2)D concentrations, as well as in urinary calcium excretion in the whole group. On the contrary, serum phosphate, PTH, and urinary phosphate excretion increased significantly. The percentage increase in PTH concentrations after phosphorus supplementation were similar in patients with optimal and suboptimal allograft function (33 vs 36%). The reduction of 1,25 (OH)(2)D concentrations after phosphorus supplementation was observed mainly in the subgroup with optimal allograft function (21% reduction with respect to baseline values), while the mean 1,25(OH)(2)D concentrations in patients with suboptimal allograft function scarcely changed (1.4% increase). Changes in 1,25(OH)(2)D concentrations after phosphorus supplementation, expressed as a percentage of the initial concentrations, correlated positively with the percentage changes in PTH concentrations for the whole group, as well as for each subgroup. The best determinants for the percentage and the absolute increase in PTH concentration after phosphorus supplementation was the final serum phosphate concentration (F=4.84, r=0.37, P=0.035) and the increase in serum phosphate (F=7.69, r=0.45, P= 0.009) respectively. CONCLUSIONS: Oral phosphorus supplementation led to a significant increase in the PTH concentration of kidney transplant recipients. The mean 1,25(OH)(2)D concentration decreased mainly in recipients with optimal allograft function. The counterbalance effect of PTH on 1,25(OH)(2)D production may account for the relative preservation of 1,25(OH)2D levels in recipients with suboptimal allograft function.

Risk factors for developing peritonitis caused by micro-organisms of enteral origin in peritoneal dialysis patients.

OBJECTIVE: To investigate the risk factors associated with the development of peritonitis caused by enteral bacteria in peritoneal dialysis patients, including the prescription of gastric acid inhibitors as a potential risk factor. DESIGN: Retrospective single-center study. SETTING: Tertiary university hospital. PATIENTS AND MAIN OUTCOME MEASURES: Fifty-five patients who entered into our continuous ambulatory peritoneal dialysis (CAPD) program during the last 6 years were included. Multiple logistic regression analysis was used to establish the best determinants over the development of at least one episode of enteric peritonitis. The predictive variables included in the model were: age, gender, diabetic versus nondiabetic, polycystic versus nonpolycystic kidney diseases, history of constipation, presence or absence of moderate/severe malnutrition, peritoneal transport characteristics, peritoneal protein losses, rate of exit-site infections, rate of total peritonitis, intestinal abnormalities, and treatment with inhibitors of gastric acid secretion. RESULTS: The total number of peritonitis episodes during the studied period was 88, which clustered in 34 of 55 patients. Fourteen (16%) were caused by enteric micro-organisms in 10 patients: Escherichia coli (6), Klebsiella sp (2), Enterobacter sp (1), and Enterococcus sp (5). Nine of 10 patients who developed enteric peritonitis were on gastric acid inhibitors (3 patients on omeprazole and 6 patients on H2-antagonists), while 15 of 45 patients who did not develop enteric peritonitis were on gastric acid inhibitors (all of them on H2-blockers). There were temporal relationships between the start of gastric acid inhibitors and the development of enteric peritonitis in 6 of 9 patients who were on this medication. Four of 10 patients who developed enteric peritonitis had diverticulosis. Ten of 45 patients who did not develop enteric peritonitis had been diagnosed with diverticulosis of the colon or sigmoid prior to entry to CAPD. The unique patient who was not on gastric acid inhibitors and developed enteric peritonitis, had been diagnosed with chronic atrophic gastritis with achlorhydria. By multiple logistic regression analysis, the treatment with gastric acid inhibitors was the only independent variable that entered into the best predictive equation over the development of enteric peritonitis (log likelihood ratio = -26.077, odds ratio = 18; 95% CI odds ratio: 2 - 155). CONCLUSION: Gastric acid inhibitors may increase the risk for developing enteric peritonitis in peritoneal dialysis patients.

[Treatment with pravastatin of dyslipidemia associated with diabetic nephropathy]. / Tratamiento con pravastatina de la dislipemia asociada a nefropatía diabética.

OBJECTIVE: Patients with type II diabetes mellitus have an increased risk of coronary he disease. We investigated the efficacy and safety of pravastatin in the treatment of patients with diabetic nephropathy and hypercholesterolemia. METHOD: In this 6-months study, 12 patients (4 men, 8 women, mean age 60.5 +/- 10.8 years), with diabetic nephropathy and hypercholesterolemia (fasting plasma low-density lipoprotein cholesterol levels -LDL-C- > 130 mg/dl) received pravastatin 10 mg/day. The dose could be doubled after 4 weeks. Seven patients have chronic renal failure. RESULTS: Significant reductions in LDL-C (-19.1%, p < 0.05), total cholesterol (-16%, p < 0.01), very-low-density lipoprotein cholesterol (-29.2%, p < 0.05), apolipoprotein B (-21.5%, p < 0.05), and triglycerides (-26.0%, p < 0.01) were noted. No changes were found either in high-density-cholesterol or its fractions (HDL2 and HDL3) or in apolipoprotein A plasmatic levels. Pravastatin was well tolerated and no one side effect was detected. No clinically significant changes on the control of diabetes, renal function, as assessed by plasmatic creatinin and creatinin clearance, and proteinuria were seen during the follow-up time. CONCLUSIONS: The results of the study demonstrate that pravastatin is well tolerated and effective in lowering total cholesterol and LDL-C in patients with diabetic nephropathy and hypercholesterolemia.