Gene/Protein Disease Symptom Drug Enzyme Compound
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Low protein diets have been used for a long time in the conservative management of chronic renal failure as they have a beneficial effect in preventing the appearance of symptoms. However, with the exception of the beneficial effect on hyperphosphatemia of the very low protein diets supplemented with ketoacids, they have no proven effects on the other aspects of the uremic syndrome. Moreover, the weight of the evidence suggests that the effect of these diets on preservation of GFR, if any, in patients with nondiabetic renal disease is small and of little clinical relevance. There is very little evidence in the literature of its role in patients with diabetes. The nutritional safety of these diets is still suspect. Patients with chronic renal failure have low energy intakes, which is further reduced when these diets are prescribed. Metabolic studies predict that these patients would be in negative nitrogen balance and in fact, even nutritionally sound, nondiabetic patients enrolled in the Modification of Diet in Renal Disease Study developed subclinical signs of malnutrition. It is possible that the nutritional decline may have been more pronounced on longer duration of follow-up. Finally, these diets are difficult to follow, leading to issues of compliance and exert a great toll on the time of the dietitians. Hence, we conclude that low protein diets are not necessary in chronic renal failure.
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PMID:Low protein diets are not needed in chronic renal failure. 1068 58

Tumor lysis syndrome is characterized by hyperuricemia, hyperkalemia and hyperphosphatemia followed by hypocalcemia. Sometimes they are accompanied by hyperglycemia. It can lead to acute renal insufficiency, neurological and cardiological disorders. In the Clinic of Paediatric Haematology and Chemotherapy in Zabrze, in the period from Jan.01, 1990 to Dec.31, 1997, 305 children were treated due to neoplastic diseases of haematopoietic system: 169 with ALL, 34--ANLL, 48--NHL and 54--HD. Tumor lysis syndrome was found in 11 children, what was 3.6% of all patients. They included 3 children with ALL/1 from group SRG and 2 with HRG/, 2 with ANLL, 6 with NHL/2 with NB-NHL and 4 with B-NHL/. Tumor lysis syndrome did not occur in any patient with HD. Two symptoms of tumor lysis syndrome were found in 13 children (4.26%) including 3 with ALL (1 SRG and 2 HRG), 2 with ANLL and 8 NHL/3-NB-NHL and 5-B-NHL/. Diabetes occurred in two children with ALL. Acute renal insufficiency occurred in 6 children with ALL, 2 with ANLL and 8 with NHL. Two patients with B-NHL required dialysis. One renal insufficiency treated with hemodialyses was the first symptom of lymphoma. To prevent the consequences of tumor lysis syndrome hydration with alkalization, constant monitoring of the above mentioned biochemical parameters are necessary. Acute renal insufficiency, not responding to conservative treatment, should be immediately treated with hemodialyses and chemotherapy should be introduced under its 'shield'.
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PMID:[Tumor lysis syndrome in the course of neoplastic disease of hematopoietic system in children]. 1073 89

Cardiovascular disease is the major cause of death in patients with end-stage renal disease (ESRD). ESRD patients are almost invariably hypertensive. They all have acquired combined hyperlipidemia and increased Lp(a), hyperhomocysteinemia, decreased physical activity, psychosocial stress, insulin resistance, procoagulant factors, left ventricular hypertrophy, and increased oxidative stress. Diabetes mellitus, a major risk factor for both cardiovascular disease and ESRD, has become the commonest cause of ESRD. If ESRD patients choose to smoke, the additive risk is profound. Moreover, ESRD patients are becoming older and are often menopausal if female. Finally, ESRD patients have a dramatic tendency for vascular and cardiac calcification, probably related to hyperphosphatemia and hyperparathyroidism. Cardiovascular disease is also a major risk in patients with decreased renal function of nearly any degree. Data from the HDFP study showed that patients with a serum creatinine concentration > 1.5 mg/dl had a profoundly higher risk of cardiovascular disease than patients with creatinine values below this value. These data were recently corroborated in the HOPE study. Microalbuminuria (MAU), with or without diabetes mellitus, indicates increased cardiovascular disease risk even without decreases in glomerular filtration rate. We found earlier that nondiabetic hypertensive patients with MAU had much higher rates of myocardial infarction, stroke, and peripheral vascular disease, than similar hypertensive patients without MAU. In conclusion, the presence of decreased renal function or MAU is a major cardiovascular risk factor. ESRD can be regarded as a catastrophic risk factor. Prophylactic measures known to be effective in reducing the risk from cardiovascular disease are grossly underused. Unfortunately, they are less effective in patients with renal disease, and new strategies are needed.
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PMID:Renal disease as a risk factor for cardiovascular disease. 1119 57

Cardiac valve calcification (VC) has long been regarded as a consequence of aging and abnormal calcium-phosphate metabolism in uremic patients. In view of the recent recognition of association among inflammation, malnutrition, and atherosclerosis, the possible role of inflammation and malnutrition in VC was investigated. Inflammatory markers (including C-reactive protein [CRP], fibrinogen, and basal metabolic rate) and nutritional status (assessed using serum albumin, subjective global nutrition assessment, and handgrip strength) were examined, in addition to calcium phosphate parameters and other traditional cardiovascular risk factors, including gender, smoking habits, BP, and lipid profile, in relation to VC in 137 patients who were on continuous ambulatory peritoneal dialysis. Compared with patients with no VC, patients with VC not only were older (60 [10] versus 54 [12] yr; P = 0.005), had higher plasma phosphate (1.89 [0.52] versus 1.64 [0.41] mmol/L; P = 0.003), and had higher parathyroid hormone (83 [40, 145] versus 38 [16, 71] pmol/L; P = 0.001) but also had higher CRP (4.5 [0.1, 13.4] versus 0.2 [0.1, 4.4] mg/L; P = 0.004), had higher fibrinogen (6.6 [1.9] versus 5.7 [1.3] g/L; P = 0.002), and had lower serum albumin (26 [4] versus 29 [3] g/L; P = 0004). Twenty-three percent of patients with VC versus 17% of patients with no VC were moderately to severely malnourished according to subjective global nutrition assessment (P = 0.05). Even after adjustment for patients' age, duration of continuous ambulatory peritoneal dialysis, diabetes, and calcium x phosphate product, cardiac VC remained strongly associated with CRP (odds ratio, 1.05; P = 0.026) and albumin (odds ratio, 0.85; P = 0.01). The data suggest that VC not only is a passive degenerative process but also involves active inflammation, similar to that seen in atherosclerosis. The presence of uncontrolled hyperphosphatemia and hyperparathyroidism further accelerates the progression of calcification. The data also indicate that VC and atherosclerosis should be considered as associated syndromes, sharing similar pathogenic mechanisms, namely active inflammation.
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PMID:Association of inflammation and malnutrition with cardiac valve calcification in continuous ambulatory peritoneal dialysis patients. 1151 87

Oral phosphosoda is increasingly being used as a bowel preparation for colonoscopy, as it requires that a much smaller volume be ingested and is equally effective and less costly than polyethylene glycol-based electrolyte solutions. Oral phosphosoda has a good safety record, but complications of its use may occur. We describe a patient who died as a result of severe hyperphosphatemia after an oral phosphosoda bowel preparation. A 55-year-old man was admitted with rectal bleeding, abdominal pain, and vomiting. He had a history of diabetes, hypertension, and end-stage renal disease and had successful renal transplant 3 years prior. His initial serum creatinine, calcium, phosphate, and electrolyte levels were normal. He vomited after polyethylene glycol-based electrolyte solution, and an alternate bowel preparation with oral phosphosoda was recommended. He received 90 mL of oral phosphosoda as a single dose. Six hours later, he had cardiorespiratory arrest and was found to have hyperphosphatemia (serum phosphate, 17.8 mg/dL), a high anion gap acidosis, hypoxia, and oliguric renal failure. Resuscitation was unsuccessful. Autopsy showed ischemic colitis. We conclude that bowel preparation with phosphosoda may be associated with severe complications and should be avoided if there is any suggestion of impaired renal function or poor gut motility.
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PMID:Fatal hyperphosphatemia from a phosphosoda bowel preparation. 1190 63

The interlinking of CVD with CKD is undeniable. CVD accounts for more than 50% of all morbidity and mortality in patients with kidney disease who have undergone renal replacement therapy, and CVD is also prevalent in patients with mild and moderately severe kidney disease. To help address the elevated risks of these patients, primary care physicians need to maintain vigilance in (1) identifying patients who have CKD and (2) implementing strategies for reducing the prevalence of CVD in this population. It is essential that patients be screened for relatively mild kidney disease by measurement of serum creatinine and urine microalbumin and by calculation of the glomerular filtration rate in mL/min/1.73 m2 using equations based on serum creatinine. Rigorous assessment of conventional risk factors, including dyslipidemia, hypertension, and diabetes, is also necessary to prevent the poor outcomes currently observed in persons with CKD. Routine use of ACE inhibitors and aspirin is encouraged in all patients with CKD, and strict glycemic and blood pressure control is recommended for optimal outcomes. In addition, patients should be screened and treated for risk factors particularly associated with kidney disease and CVD morbidity and mortality, including anemia, hyperphosphatemia, and hyperparathyroidism. Finally, physicians should be careful to avoid therapeutic nihilism in patients with kidney disease; those at highest risk of CVD are likely to receive the greatest benefit from cardiovascular therapies.
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PMID:Cardiovascular disease and the kidney. Tracking a killer in chronic kidney disease. 1198 33

Calciphylaxis is a small vessel vasculopathy involving mural calcification with intimal proliferation, fibrosis, and thrombosis. This syndrome occurs predominantly in individuals with renal failure and results in ischemia and necrosis of skin, subcutaneous fat, visceral organs, and skeletal muscle. The syndrome causes significant morbidity in the form of infection, organ failure, and pain. Mortality rates are high. In individuals with renal failure, risk factors for the development of calciphylaxis include female sex, Caucasian race, obesity, and diabetes mellitus. Many cases occur within the first year of dialysis treatment. Several recent reports demonstrate that prolonged hyperphosphatemia and/or elevated calcium x phosphorus products are associated with the syndrome. Protein malnutrition increases the likelihood of calciphylaxis, as does warfarin use and hypercoagulable states, such as protein C and/or protein S deficiency. Recent advances in diagnostic tools and therapeutic strategies have helped in the management of patients with calciphylaxis.
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PMID:Calciphylaxis: emerging concepts in prevention, diagnosis, and treatment. 1210 Apr 55

Vascular calcification is a frequent complication of uremic patients. In addition to classical risk factors such as age, male gender, smoking, inflammation, hypertension, dyslipidemia, and diabetes, which also exist in the general population, patients with chronic renal failure have other risk factors such as oxidative stress, inflammation, hyperparathyroidism, hypoparathyroidism, hypercalcemia, hyperphosphatemia, and overtreatment with calcium and vitamin D. These latter risk factors may even have a better predictive value than classical risk factors for coronary heart disease in uremic patients.
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PMID:Advanced oxidation protein products, parathyroid hormone and vascular calcification in uremia. 1220 1

Hyperparathyroidism (HPT) is common in patients on dialysis, and parathyroidectomy (PTx) is often required. We present a retrospective, descriptive analysis of data corresponding to 148 patients on dialysis undergoing PTx due to severe refractory HPT (PTH 1401 +/- 497 pg/mL, Ca 10.6 +/- 0.8 mg/dL, P 6.9 +/- 1.7 mg/dL). Demographic data were compared with those recorded in 309 patients on dialysis not subjected to PTx who were managed at the same hospital. In the PTx group, the factors age (49.3 +/- 14 years), male gender (48.6%), and diabetes (0.7%) were significantly lower than in the non-PTx group (61.5 +/- 14.9 years, male gender 59%, diabetes 19.4%), while time on dialysis was longer (8.6 +/- 5.8 vs. 5.5 +/- 5.4 years). In 129 of the study patients (87.4%), four or more glands were identified, and total PTx plus autotransplantation (AT) in the forearm was performed. In the remaining 19 patients, two to three glands were identified, and AT was not undertaken. Four of the 19 patients were successfully operated on again for persistent HPT, seven showed PTH levels <250 pg/mL, and eight maintained severe HPT. Perioperative complications included one death due to cardiac insufficiency, two repeat operations due to bleeding, and one patient with chronic hoarseness. Hospital stay was prolonged in 20% of patients due to a hungry bone syndrome. Among those patients with PTx and AT, HPT recurred in 21 patients (16.2%) at 3.1 +/- 2.3 years. In 13 of these patients, autograft was removed at 7.5 +/- 2.9 years. Serum calcium and phosphate levels improved after PTx, and these results were maintained for 5 years (9.6 +/- 0.8 and 4.2 +/- 1.2 mg/dL, respectively). In conclusion, PTx with AT is a safe option for the treatment of severe HPT that is accompanied by low morbidity and mortality and a good outcome. Medical treatment should not be prolonged at the expense of long repeated bouts of hypercalcemia and/or hyperphosphatemia with their irreversible consequences.
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PMID:Parathyroidectomy: whom and when? 1275 76

Arteriosclerosis, atherosclerosis and vascular calcification are causally related to the high morbidity and mortality of patients with chronic renal failure. Oxidative stress and carbonyl stress of uremia, dialysis procedure and/or intravenous iron therapy result in AGE (advanced glycation end-product), ALE (advanced lipoxidation end-product) and AOPP (advanced oxidation protein product) formation, favouring together with elevated CRP (C-reactive protein) levels the development of cardiovascular and cerebrovascular complications. Enhanced plasma levels of homocysteine and ADMA (asymmetric dimethylarginine) contribute to this process. In addition, in chronic renal insufficiency hyperphosphatemia and an enhanced calcium x phosphorus ion product are associated with the morbidity and mortality of the patients, particularly in the presence of fetuin deficiency. Phosphorus, AGEs and AOPPs, beside other factors, catalyze the conversion of vascular smooth muscle cells to osteoblast--like cells (particularly in the presence of monocytes/macrophages), resulting in bone matrix protein formation. Other risk factors, such as age, male sex, smoking, hypertension, diabetes, chronic inflammation, insulin resistance or dyslipidemia (enhanced non-HDL-cholesterol) also contribute to the atherosclerotic risk profile of the patient with chronic renal insufficiency. While there is growing understanding of the mechanisms involved in arteriosclerosis, atherosclerosis and vascular calcification in uremia, we are still missing effective therapeutic maneuvers for reduction of excess mortality in uremic patients.
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PMID:[Atherosclerosis and uremia: signifance of non-traditional risk factors]. 1277 74


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