[Carotid ultrasound: prevention of heart disease and mortality on haemodialysis]. / La ecografía carotídea es útil para predecir enfermedad coronaria y mortalidad en pacientes en hemodiálisis.

INTRODUCTION: Cardiovascular disease and other complications of atherosclerosis are the most common cause of death in patients with chronic renal failure in maintenance hemodialysis (MHD). Carotid ultrasonography is a simple non-invasive tool to investigate the vascular system, by means of intima media thickness (IMT) measurement and carotid wall calcifications. OBJECTIVE: To determine IMT and the presence of plaques, and their possible clinical relationships; finally we tried to investigate whether they would predict cardiovascular morbidity and mortality in patients in MHD. METHODS: We studied 60 MHD patients (age 68 +/- 13 years, 48% male, 50% diabetics, time on MHD 32 +/- 11 months) and a control group of 274 people matched for age and sex. Follow-up period was 66 +/- 13 months. MEASUREMENTS: Demographic and clinical data, serum levels of homocysteine (tHcy), folic acid (FA) and B6 and B12 vitamins. IMT was measured by high-resolution B-mode ultrasonography. RESULTS: IMT was higher in MHD patients than in those in the control group (0.947 +/- 0.308 vs 0.619 +/- 0.176 mm; P < 0.001). IMT was related with age (r = 0.268; P = 0.038), diabetic (r = 0.650; P < 0.001) and hypertensive condition (r = 0.333; P = 0.012), but not wih lipids, tHcy or FA. Patients who suffered from coronary artery disease, peripheral artery disease or stroke had higher IMT than those without those events (1.156 +/- 0.371 vs 0.875 +/- 0.285 mm; P < 0.001; 1.205 +/- 0.374 vs 0.911 +/- 0.231 mm; P = 0.007; 1.195 +/- 0.264 vs 0.844 +/- 0.251; P < 0.001 respectively). Something similar occurred with the presence of plaques. During the follow-up period 36 patients died (60%), 67% of them due to cardiovascular causes. IMT was higher in patients who died than those who survived (1.020 +/- 0.264 vs 0.858 +/- 0.334 mm; P = 0.044). The survival rate during the observation period was significantly lower in the final IMT fourth (20%) than in the first (72%) (P = 0.014). The presence of carotid plaques was an independent predictor of cardiovascular mortality. CONCLUSIONS: These findings suggests that measurement of carotid IMT and the presence of wall plaques are useful tools to predict cardiovascular events and mortality in patients in MHD.

[Changes in mineral metabolism in stage 3, 4, and 5 chronic kidney disease (not on dialysis)]. / Alteraciones del metabolismo mineral en la enfermedad renal cronica estadios III, IV Y V (no en dialisis).

UNLABELLED: With progression of chronic kidney disease (CKD), disorders of mineral metabolism appear. The classic sequence of events begins with a deficit of calcitriol synthesis and retention of phosphorus. As a result of this, serum calcium decreases and parathyroid hormone (PTH) is stimulated, producing in the bone the high turnover (HT) bone disease known as osteitis fibrosa while on the other extreme we find the forms of low turnover (LT) bone disease. Described later and initially associated with aluminum intoxication, these diseases are now seen primarily in older and/or diabetic patients, who in a uremic setting have relatively low levels of PTH to maintain normal bone turnover. Osteomalacia is also included in this group, which after the disappearance of aluminum intoxication is rarely observed. LT forms of hyperparathyroidism facilitate the exit of calcium (Ca) and phosphorus (P) from bone, whereas the adynamic bone limits the incorporation of Ca and P into bone tissue. Therefore, both forms facilitate the availability of Ca and P, which ends up being deposited in soft tissues such as arteries. The link between bone disease and vascular calcifications in CKD is now a well-established phenomenon. 2. Diagnostic strategies Calcium, Phosphorus They have little capacity to predict underlying bone disease, but their regular measurement is decisive for therapeutic management of the patient, especially in the dose titration stages of intestinal phosphorus binders, vitamin D analogs or calcimimetics. Ideally, Ca++ should be used, but total Ca is routinely used. It is recommended to adjust albumin levels in the event of hypoalbuminemia (for each g/dL of decrease in albumin, total serum Ca decreases 0.9 mg/dL). The following formula facilitates rapid calculation of corrected total calcium: Corrected total Ca (mg/dL) = total Ca (mg/dL) + 0.8 [4-albumina (g/dL)]. Parathyroid hormone "Intact" PTH is the biochemical parameter that best correlates with bone histology (levels measured with the Allegro assay from Nichols Institute Diagnostics, no longer available). Various assays are currently available that use antibodies against different fragments of the molecule, but they have significant intermethod variability and have not been validated. A whole PT assay (1-84) is currently unavailable. A consensus to establish uniform criteria for PTH measurement remains to be established. During the dose titration stages of intestinal phosphorus binders, vitamin D analogs or calcimimetics, more frequent measurement may be required based on clinical judgment. Calcifediol (25(OH)D3) It is important to maintain adequate levels of 25(OH)D3 (> 30 ng/mL), since they will be the substrate for production of 1- 25(OH)2 D3, and their deficiency aggravates hyperthyroidism. Determining 25(OH)D3 levels every 6-12 months is a recommended guideline. Other markers of bone turnover (osteocalcin, total and bone alkaline phosphate, free pyridolines in serum, and C-terminal telopeptide of collagen) do not improve the predictive power of PTH and therefore their systematic use is not justified. Radiologic studies Radiologic studies are of little diagnostic utility, because biochemical changes precede radiologic changes. Systematic radiologic evaluation of the skeleton in asymptomatic patients is not justified at present. They are useful as the first step in the study to detect vascular calcifications and amyloidosis due to b2-microglobulin and in symptomatic and at risk patients to detect vertebral fractures. Bone densitometry: Dual energy x-ray absorptiometry (DEXA) is the standard method to determine bone mineral density (usually in the femoral neck and vertebrae). It provides information on changes in bone mineral content, but not on the type of underlying bone disease. It is useful for follow-up of bone mass or for the study of bone mass changes in the same patient. Its value as a predictor of the risk of fracture has not been demonstrated in patients on kidney replacement therapy or with advanced chronic kidney disease. It is indicated in patients with fractures or risk factors for osteoporosis. Bone biopsy: The "gold standard" for diagnosis of bone disease. With improved knowledge of the value of noninvasive parameters, its use is infrequent. INDICATIONS: Pathological fractures in the presence or absence of minor trauma. Symptomatic patients in the presence of incongruent clinical parameters. A typical case is the presence of unexplained hypercalcemia from systemic disease, with inconclusive serum PTH values (between 120-450 pg/mL as an estimated range). Evaluation and follow-up of cardiovascular calcifications There are no consensuated clinical practice guidelines for the evaluation and follow-up of extraosseal calcifications in CKD. The clinical tools for evaluation and follow-up of cardiovascular disease are used based on clinical judgment. The periodicity of follow-up has not been established . 3. Recommended biochemical values The biochemical values recommended in clinical practice guidelines for the evaluation of bone mineral metabolism are summarized in Figure 3. The recommended PTH values do not fully coincide with the K/DOQI guidelines. The wide variability in PTH values depending on the assays used has led us to expand the recommended PTH range in stage 3 and 4 CKD. 4. Treatment 4.1. Diet. The recommended diet for the patient with CKD is traditionally based on protein restriction and phosphorus restriction for control of mineral metabolism. A favorable circumstance is that there is a close relationship between protein and phosphorus intake. In CKD stages 3, 4 and 5, it is recommended to restrict phosphorus intake to between 0.8-1 g/day when serum levels of phosphorus and PTH are above the recommended range. This is approximately equivalent to a diet of 50-60 g of protein. This reasonable antiproteinuric strategy that also restricts phosphorus intake is nutritionally safe. What should we tell them to eat? In a practical and oversimplified way, we recommend the following daily intake: Animal proteins: 1 serving (100-120 g), dairy products: 1 serving (equivalent to 200-240 mL of milk or 2 yoghourts), bread, cereals, pastas (1 cup of pasta, rice or legumes + some bread or cookies), vegetables and fruits relatively freely, but with moderation. 4.2. Medication Vitamin D supplements should be provided if serum levels are less than 30 ng/mL. In Spain, vitamin D3 (cholecalciferol) is marketed as Vitamin D3 Berenguer 2,000 IU/mL of solution. Combinations of calcium with cholecalciferol are also available. Most of the dosage forms contain approximately 500 mg of Ca+ and 400 IU of cholecalciferol. Alternatively, calcifediol (25(OH)D3), as Hidroferol 100 mcg/mL, has been used, although the dose range is very variable and has not been established. 4.3. Phosphorus binders. Use if hyperphosphatemia occurs. Start with calcium-containing phosphorus binders (calcium carbonate or calcium acetate), which also provide calcium if dietary intake is inadequate. Do not exceed 1.5 g of Ca++ per day. The most used are calcium carbonate and calcium acetate. Calcium acetate shows a similar binding potency to calcium carbonate but with a lesser calcium overload, and thus would have certain advantages as well as its greater effect at different pH ranges. However, gastric intolerance is more frequent with this dosage form. Aluminum hydroxide may sometimes be required to control phosphoremia or the occurrence of hypercalcemia. Serum aluminum values should be maintained below 30 mcg/L. Avoid use for longer than 6 months and daily doses greater than 1.5 g. Sevelamer is associated with an increased risk of acidosis and has not been approved for use in predialysis stages. Lanthanum carbonate has been recently marketed in Spain, although its indication for use in the predialysis stage of CKD is still not approved. 4.4. Vitamin D derivatives. Indicated when PTH levels are elevated. A prerequisite for their use is that Ca and P serum levels are adequately controlled. Vitamin D derivates available in Spain are 1,25(OH)2D3 (Calcitriol)and 1a(OH)D3 (a-Calcidiol). Doses should be titrated until PTH levels are normalized. Phosphate binder doses often need to be increased because these vitamin D derivatives increase intestinal absorption of calcium and phosphorus. Low doses do not cause hypercalcemia or hyperphosphatemia and do not worsen the course of renal function. Recommended doses: Calcitriol 0.25 mcg every 48 hours and alpha-Calcidiol 0.50 mcg every 48 hours. Soon to be available on the Spanish market is the oral dosage form of paricalcitol (recommended initial dose of 1 mcg/24 h), with a lesser hypercalcemic and hyperphosphoremic effect. Clinical use of calcimimetics in the predialysis state is not yet recommended and is currently under investigation.

[Nutrition guidelines for advanced chronic kidney disease (ACKD)]. / Guia de nutricion en enfermedad renal cronica avanzada (ERCA).

Prescription of protein intake in CKD is complicated by potential conflicts between goals to delay progression of CKD and preserve nutritional status. Providing a protein intake of about 0.75 g/kg/day appears reasonable in patients with GRF > 30 mL (CKD stages 1-3). In CKD stage 4 and 5, it is recommended to provide a protein intake of about 0.6 g/kg/day to slow progression and minimize accumulation of uremic toxins. - Maintaining adequate energy intake is essential in all stages of CKD. - Assessment of nutritional status in CKD requires multiple markers to assess protein status, fat stores, body composition, and protein and energy intake. - PEM can be considered as an indication for the initiation of kidney replacement therapy. If PEM develops or persists despite attempts to optimize intake, and there is no apparent cause for malnutrition other than intake or anorexia, initiation of dialysis or kidney transplant is indicated in patients with GFR > 15 mL/min. - Nutritional treatment for patients with CKD should include nutritional assessment and education and nutritional planning and follow-up.

[The challenge of hyperphosphatemia control in chronic kidney disease]. / El reto del control de la hiperfosfatemia en la enfermedad renal crónica.

Mineral metabolism abnormalities in chronic kidney disease (CRK) have adverse effects, particularly on the skeleton and cardiovascular system. Among the classic biochemical abnormalities, hyperphosphoremia plays a significant role. It stimulates parathyroid hormone production by the parathyroid gland both directly (it increases PTH synthesis and secretion and induces cell proliferation) and indirectly (it suppresses calcitriol synthesis by the kidneys and reduces vitamin D receptor and calcium sensor expression). It induces phenotypical activation of vascular smooth muscle cells, causing them to acquire an osteoblastic profile and produce procalcifying factors. As a result of both effects, numerous studies (retrospective) have shown an increase in mortality associated with hyperphosphoremia (usually P > 5.5 mg/dL). Finally, recent observations suggest a direct association between phosphoremia and CKD.Undoubtedly, all these are powerful arguments in favor of increasingly strict control of P in CKD.

[A study using nondecalcified bone biopsy of the incidence and presentation forms of renal osteodystrophy]. / Estudio con biopsia ósea sin descalcificar de la incidencia y formas de presentación de la osteodistrofia renal.

BACKGROUND: Renal osteodystrophy (ROD) is a common complication of chronic renal failure. Fibrous osteitis and, to a lesser extent, osteomalacia are the predominant lesions. The aim of the present study was to evaluate the prevalence of the different forms of ROD. METHODS: Nondecalcified bone biopsies were evaluated in 100 patients with end-stage renal disease (57 in pre-dialysis and 43 on hemodialysis) in whom biochemical (calcium, phosphorus, alkaline phosphatase, parathyroid hormone) and histomorphometric studies were carried out. Bone biopsies were classified in four histological groups: mild, fibrous osteitis (FO), osteomalacia (OM) and mixed type (FO + OM). RESULTS: 96% of patients had histological findings of ROD with the following distribution: 41% mild; 30% FO; 14% OM; and 11% mixed. The most advanced types of ROD were seen in interstitial renal diseases. Pre-dialysis OM was associated with metabolic acidosis, a low phosphocalcic product and relative hypophosphoremia. Chronic aluminium poisoning was uncommon (7%) and was basically associated with OM. No instance of aluminium poisoning with osteodystrophy and bone fractures was seen. CONCLUSIONS: The most severe histological forms of OM were found in hemodialysis patients with persistent hypophosphoremia and associated with osteosclerosis.

[Recovery of kidney function in a female patient with severe lupus nephropathy]. / Recuperación de la función renal en una paciente con nefropatía lúpica severa.

The evolution of Lupus Nephritis to end-stage chronic renal failure is a frequent event. We report the case of a 28 years old patient with diffuse proliferative lupus nephritis with crescents formation and rapid decline of renal function without response to steroids, immunosuppressors and plasmapheresis. After 10 weeks of continued hemodialysis, during which the patient received 30 mg of prednisone in alternate days, renal function recovered spontaneously, and after 1 year of follow-up plasma creatinine is maintained in 2.5 mg/dl.

Osteomalacia in chronic renal failure before dialysis.

Bone biopsies taken from 327 patients before the start of dialysis have been correlated with clinical and biochemical findings to test various theories about the aetiology of osteomalacia. Two groups of patients, 100 with osteomalacia and 100 with pure osteitis fibrosa, have been compared in detail. Osteomalacia is associated with chronic pyelonephritis or obstruction as primary renal disease, and with acidosis, hypocalcaemia and normophosphataemia (as opposed to hyperphosphataemia). We have found no association between osteomalacia and known duration or severity of uraemia and in a small series of observations we have not confirmed previous reports of a close association between osteomalacia and depressed plasma 25(OH) cholecalciferol values.