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Ocular complications are frequent in chronic renal failure patients treated with maintenance hemodialysis (HD) and in renal allograft recipients. Headache, nausea and fatigue sometimes develop in combination with a rise in intraocular pressure (IOP). We did not find statistically significant differences in IOP before and after HD. There was no correlation between changes in IOP during HD and the decrease in systolic and diastolic blood pressure or decrease in body weight. No patient had borderline or elevated IOP following HD. Due to improved dialytic techniques a significant rise in IOP during HD rarely occurs anymore.
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PMID:Intraocular pressure in chronic renal failure patients treated with maintenance hemodialysis. 938 Mar 46

In 25 patients with chronic renal failure treated by haemodialysis with acetate-37 mEq/l containing fluid, plasma free, total carnitine and acetate concentration before and after HD were assessed. The concentration of acetate was high-12 mmol/l in 4 patients in which carnitine concentration was low. In these patients the incidence of the so-called "dialysis intolerance" or "acetate intolerance" such as acute hypotension, nausea, vomiting and headache were increased. The correlation between the serum acetate level and carnitine level and the symptoms suggest that the acetate overload during acetate dialysis affects acetate metabolism and administration of L-carnitine decreases the amount of accumulated acyl-CoA in the cytosol, and consequently--the citrate cycle function increases and diminish the intolerance symptoms.
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PMID:[Protective role of carnitine in acetate metabolism of patients with uremia treated by hemodialysis]. 944 Dec 89

The low-protein diet (LPD) is used in patients with advanced chronic renal failure (CRF) to improve their symptoms and decrease the progression of CRF. LPD entails the risk for caloric malnutrition, which increases protein catabolism. Two groups were obtained from a total of 33 patients with CRF with LPD (0.6 g protein/kg/day): control group (group C), which went on with the same diet, and a group S, in which a portion of proteins and calories were provided through a low-protein and hypercaloric supplement (Suplena). During 6 months the protein intake and the evolution of the nutritional status and renal function were studied and compared between both groups. Additionally, tolerance and secondary effects of the supplement were studied in group S. Twenty-two patients (eleven in each group) completed the six month follow-up. At the end of the study, group S had the nutritional parameters better preserved, came closer to the low-protein diet objective, had a better compliance with therapy and had a less marked decrease in renal function--as measured by creatinine clearance--than group C. Tolerance to supplement was good in more than 70% of patients and secondary effects--nausea, vomiting and loss of appetite--occurred in 18% of patients at the end of the 6 months. We conclude that the use of this supplement in an LPD is usually well tolerated, enhances the compliance with the diet and can be of benefit for the mebacolic-nutritional status.
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PMID:[Treatment with low-protein diet and caloric supplements in patients with chronic kidney failure in predialysis. Comparative study]. 1111 1

Protein energy malnutrition in dialysis patients has been well-described in the literature. Most malnourished patients with end stage renal disease (ESRD) suffer from a mixed marasmus-kwashiorkor type of malnutrition with loss of both somatic and visceral protein mass. Malnutrition is associated with increased risk of morbidity and mortality. Up to 50% of patients on dialysis have protein energy malnutrition (Mortelmans & Vanholder, 1999). Malnutrition may be under-recognized and under-reported in dialysis patients. Malnutrition may result from inadequate food intake secondary to the uremic condition, nausea, vomiting, loss of appetite, altered taste and other physiologic conditions that impede food intake or metabolism. The usual indices of nutritional assessment--body weight, body mass index (BMI), anthropometrics, etc., may be inaccurate in patients with ESRD, as the results are often skewed by fluid retention. Therefore, we often rely on weight loss, bloodwork, a pre-dialysis low serum potassium, phosphorus and urea, as early signs of a decreased food intake. When patients are malnourished, measures such as oral supplements and/or tube feedings may be used to augment protein and calorie intake. However, when these interventions are inadequate to reverse the malnutrition condition, intradialytic parenteral nutrition (IDPN) should be implemented. Although there is no definite supportive data to show that the use of IDPN improves morbidity and mortality of dialysis patients, there are data to support that IDPN has positive effects on numerous nutritional parameters (Acchiardo, 2000; Capelli et al., 1994; Foulks, 1999; Hiroshige et al., 1998; Ikizler et al., 1995; Korzets et al., 1999; Mortelmans & Vanholder, 1999; Saunders et al., 1999; Smolle et al., 1995). In this article, we will discuss the causes of malnutrition in dialysis patients, the use of IDPN on one of our patients, and the potential complications associated with IDPN.
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PMID:The use of intradialytic parenteral nutrition to treat malnutrition: a case study. 1453 27

Ferric gluconate complex in sucrose (Ferrlecit) has been associated with less side-effects than iron dextran; however, the recommended dose of 62.5-125 mg per treatment is only suitable for haemodialysis (HD) patients. We retrospectively analysed the incidence of the side-effects associated with a high dose of Ferrlecit infusion (20 treatments in 13 patients; 10 treatments of 250 mg/3-4 h, and 10 treatments of 500 mg/5 h infusion). The patients were in the age range of 32-75 years old, seven with chronic renal failure (CRF), and six on dialysis treatment. One (10%) of the 10 treatments using a 250 mg dose was complicated with severe nausea/vomiting, diarrhoea and a burning sensation in the feet. Three (30%) of the 10 treatments using a 500 mg dose were complicated with: chills, severe nausea/vomiting, hypotension and syncope in one; severe nausea/vomiting, diarrhoea and hypotension in one; and an episode of vomiting in one patient. A single treatment with a 250 mg dose resulted in no significant change in haematological parameters. A single treatment with a 500 mg dose resulted in a significant increase in haemoglobin (Hgb) and haematocrit (Hct), but only a rising trend in serum iron,% transferrin saturation and ferritin pre versus 1-2 months postinfusion. In conclusion, Ferrlecit doses of 250 or 500 mg are complicated with significant untoward reactions in 10-30% of patients, in a dose-dependent fashion.
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PMID:Incidence of side-effects associated with high-dose ferric gluconate in patients with severe chronic renal failure. 1499 10

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.
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PMID:Hyperparathyroidism. 1524 24

(1) Patients who require dialysis for chronic renal failure develop phosphocalcium metabolic disorders that often lead to secondary hyperparathyroidism. Standard treatment consists of a phosphate chelator and vitamin D, along with the use of an appropriate calcium concentration in the dialysis bath, but is difficult to manage. (2) Parathyroid cancer is a rare malignancy frequently associated with hypercalcaemia. (3) Cinacalcet is a calcimimetic agent that reduces the parathormone level. Clinical evaluation includes more than a dozen dose-finding studies and clinical trials. The optimal dose seems to range from 30 to 180 mg/day and varies widely from one patient to another. (4) 3 double-blind placebo-controlled trials, lasting for a maximum of one year and involving a total of 1136 dialysis patients with chronic renal failure, showed no improvement in quality of life with cinacalcet. The target parathormone level was reached by 40% of patients on cinacalcet versus 5% of patients on placebo, while the effects of cinacalcet on calcium levels (-7%) and phosphate levels (-8%) were modest. No impact on bone complications is mentioned in available reports. (5) The assessment of treatment of parathyroid cancer is limited to one ongoing non comparative trial involving 21 patients. (6) During clinical trials, 11% of dialysis patients had low parathormone levels, creating a risk of adynamic bone disease and fractures, but available data are sparse. (7) Two-thirds of patients receiving cinacalcet have episodes of hypocalcaemia, which may in part account for reports of seizures (1.4% of patients), nausea (31%) and vomiting (27%). Many adverse effects seen in animal studies have not been adequately investigated in the clinical setting, such as an increase in the QT interval, thyroid disorders, and sexual dysfunction. Cinacalcet is a powerful CYP 2D6 inhibitor and is also metabolised by isoenzymes CYP 3A4 and CYP 1A2, creating an increased risk of drug interactions. (8) In practice, treatment with cinacalcet seems difficult to manage and to provide only limited benefits. Available assessment reports leave many questions unanswered, and this is a further reason not to use this product outside of clinical trials, either after failure of phosphate chelator and vitamin D therapy (especially as an alternative to surgery) or in parathyroid cancer.
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PMID:Cinacalcet: new drug. Secondary hyperparathyroidism: where are the clinical data? 1676 95

Hemolytic uremic syndrome is caused primarily by Shiga toxin-producing Escherichia coli O157:H7. The most common cause of acute renal failure in children, hemolytic uremic syndrome also can occur in adults. Characteristic features of the syndrome are microangiopathic anemia, thrombotic thrombocytopenia, and renal failure. Although the presentation of this syndrome is diverse, the classic prodromal illness is bloody diarrhea following ingestion of hamburger meat contaminated with E. coli O157:H7, the most common mode of infection in the United States. Children with hemolytic uremic syndrome generally present with gastroenteritis complaints (e.g., abdominal pain or tenderness, nausea or vomiting, fever, anemia); affected adults may be asymptomatic. Complications from hemolytic uremic syndrome can include intussusception, chronic renal failure, and seizures in severe cases. Because an incubation period of approximately one week occurs between the start of diarrhea and the onset of hemolytic uremic syndrome, physicians should maintain a high index of suspicion; early laboratory testing is important to diagnose and manage this syndrome. Obtaining a complete blood count and stool culture and performing Shiga toxin testing are the first of a series of tests that may help diagnose hemolytic uremic syndrome.
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PMID:Hemolytic uremic syndrome: an emerging health risk. 1700 34

Patients with high fever and multiorgan involvement were investigated for the determination of frequency, clinical course and complications of leptospirosis in Istanbul. Leptospirosis was determined in 22 cases among the 35 hospitalized patients that were pre-diagnosed as leptospirosis according to 'Probable Leptospirosis Diagnosis and Follow-up' form. Among the leptospirosis cases 19 were male and 16 were military staff. Mean age was 35.6 y. Dark field examination (DFE), latex agglutination test (LAG), ELISA IgM, leptospirosis culture (LC) and microscopic agglutination test (MAT) were performed to confirm the diagnoses. The most frequent initial symptoms and findings were fever, fatigue, headache, nausea-vomiting and increased muscle sensitivity. Jaundice was noted only in 2 cases. A 74-y-old female patient died after the recurrence of the disease with severe rhabdomyolysis and pulmonary failure. Sagittal sinus thrombosis, perimyocarditis and chronic renal failure were major complications in another 3 patients. ELISA IgM, LC, DFE, LAG and MAT tests were positive in 68, 72, 82, 100 and 100% of the patients, respectively. As a conclusion, diagnosis of leptospirosis is usually overlooked. Clinical awareness, use of probable leptospirosis diagnosis forms and the application of different laboratory methods in the diagnosis of suspected cases may offer the chance to diagnose the leptospirosis accurately.
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PMID:Leptospirosis in Istanbul, Turkey: a wide spectrum in clinical course and complications. 1700 27

(1) In dialysis patients with chronic renal failure, hyperphosphataemia can cause osteorenal dystrophy, leading to bone pain, fractures and excess cardiovascular mortality. In addition to a low-phosphorus diet and dialysis, phosphorus chelators are usually needed to control blood phosphorus levels. The first choice is calcium carbonate, and sevelamer is an alternative. (2) Lanthanum carbonate, a phosphorus chelator, is now also licensed for the treatment of hyperphosphataemia in dialysis patients with chronic renal failure. (3) In addition to three dose-finding placebo-controlled studies, clinical evaluation includes 2 comparative randomised unblinded trials: one 6-month trial versus calcium carbonate and a 2-year trial versus other phosphorus chelators. During these trials, lanthanum was no more effective than the comparators in terms of effects on the mortality rate, incidence of fractures, or blood phosphorus level. (4) During these trials, adverse events attributed to treatment were more frequent with lanthanum than with the other phosphorus chelators. The main problems were gastrointestinal disorders (nausea, vomiting, diarrhoea, constipation and abdominal pain), headaches, seizures, and encephalopathy. (5) The accumulation of lanthanum in the bones and brain is troubling. The known long-term adverse effects of aluminium, another trivalent cation with weak gastrointestinal absorption, suggest that caution is also required with lanthanum. (6) In practice, when a phosphorus chelator is needed to treat hyperphosphataemia in dialysis patients with chronic renal failure, calcium carbonate is the first choice and sevelamer remains the best alternative.
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PMID:Lanthanum: new drug. Hyperphosphataemia in dialysis patients: more potential problems than benefits. 1745 39


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