Renal bone disease

Advances in the last few years have led to an understanding of some of the mechanisms by which renal bone disease arises with the result that, despite their complexity, the objectives of treatment and the way in which these might be realized have become more accurately defined.     

Renal involvement in Fabry disease

BACKGROUND: Fabry disease is an X-linked recessive lysosomial storage disorder that is caused by deficient activity of alpha galactosidase A. Renal involvement occurs generally in hemizygous forms. AIM: We report one case of renal involvement in Fabry disease. CASE REPORT: A 47 year-old-man had focal and segmental glomerulosclerosis with moderate renal failure. As the patient presented history of acroparesthesias, hearing loss, left ventricular hypertrophy with arrhythmia and corneal deposits, hemizygous Fabry disease was suspected. This diagnosis was confirmed with low alpha galactosidase activity. After a follow up of 5 years, the renal function remains stable but the patient died by cardiac arrhythmia. CONCLUSION: Occurrence of a glomerulonephritis associated with an hypertrophic cardiopathy without hypertension should advocate Fabry disease.     

Renal disease and the heart.

Cardiovascular disease is responsible for significant morbidity and mortality in renal failure with increased prevalence of hypertension, left ventricular hypertrophy, ischaemic heart disease and valve disease. Optimum blood pressure control is fundamental to the management of these patients but the role of secondary prevention remains poorly defined.     

Alcohol and bone disease

Alcohol is considered to be an important risk factor for various bone diseases but recent studies have shown that moderate alcohol intake can be beneficial to bone structure. Alcohol decreases osteoblastic activity, leading to decreased bone formation and defective mineralization. The changes reported in calciotropic hormones, mainly vitamin D and parathyroid hormone, are observed due in part to a deficient intestinal absorption of vitamin D and an inadequate synthesis of its hepatic metabolite, although greater emphasis has been given to dietary deficiencies or lack of exposure to sun. The changes in parathyroid hormone are not consistent and since there is no greater incidence of hyperparathyroidism in alcoholic patients, it suggests that alcohol does not have a long-term effect on the parathyroid glands. Alcohol increases calcitonin secretion acutely; calcitonin is an inhibitor of bone resorption and may be the mechanism by which moderate alcohol intake protects bone structure. Alcohol increases urinary calcium, magnesium and zinc excretion. Zinc deficiency has been postulated as a cause of oesteoporisis because it causes hypogonadism. The decrease in the levels of the gonadal hormones and the increase of cortisol, observed in chronic alcoholics, may indirectly cause osteopenia and aseptic necrosis. To these actions must be added the acidosis due to alcohol and the greater tendency of the alcoholic to fall, all of which influence bone changes and increase the incidence of bone fractures.     

Parenteral nutrition-related bone disease.

Parenteral nutrition (PN)-related bone disease remains a problem in patients of all ages. Understanding of the pathogenesis of PN-related bone disease is complicated by the effect of underlying illnesses, therapeutic interventions, and pre-existing nutrition deficiencies before the initiation of PN therapy. Interrelation of various nutrients, for example, calcium, phosphorus, and vitamin D, in their effects on bone mineralization, demands simultaneous assessment of the role of multiple nutrients and increases the difficulty in defining the role of a single nutrient in the development of bone disease. However, recent reports indicate that there exist a number of factors important in the development of PN-related bone disease and some factors such as increased mineral requirement are unique to growing infants whereas other factors such as aluminum toxicity may be common to both adult and pediatric populations. Nonnutritional factors, including chronic use of potent loop diuretics and altered acid-base status, can affect urine mineral loss, cell metabolism, and bone mineralization, particularly in small, preterm infants. Current evidence indicates that the cause of PN-related bone disease is multifactorial, and the prevention of PN-related bone disease awaits better delineation of the exact sequence of pathogenic events.     

Renal disease in the Aboriginal community of Woorabinda

OBJECTIVE: An apparent increase in the incidence of end-stage renal disease had been observed in the Australian Aboriginal community of Woorabinda. This study documents the incidence of end-stage renal disease (ESRD) in Woorabinda, and correlates this with predictors of renal disease. DESIGN: The methodology included a retrospective audit of deaths from, and cases commencing treatment for ESRD between 1999 and 2001 in Woorabinda, and a cross-sectional study. PARTICIPANTS: The 183 participants were Aboriginal residents over 15 years of age. Females numbered 102 (55.7%) and males 81 (44.3%). MAIN OUTCOME MEASURE: The incidence of ESRD was comparable to other recognised high incidence Indigenous communities in Australia. This was corroborated by a high prevalence of predictors of renal disease. RESULTS: Audit: the year 2001 age- and sex-standardised incidence ratio for commencement of renal replacement therapy is 93.18 (95% CI, 25.34-238.53). Clinical Study: the prevalence of overt albuminuria was 7.6%; 11.7% had an albumin : creatinine ratio >3.4-33.9 g mol(-1); 33.3% had microalbuminuria of > or =20 mg L(-1); and 67.8% prevalence of proteinuria was found. The prevalence of diabetes was 18.6%, with another 13.2% having impaired fasting glucose. There was a 19.7% prevalence of hypertension. Of those with hypertension 22.2% had overt albuminuria. CONCLUSIONS: Although Woorabinda was previously placed in a region of low end-stage renal disease incidence, further investigation has identified a high incidence of renal disease, not exclusively due to diabetes. The finding raises questions regarding the current trajectory of the epidemic in other Aboriginal and Torres Strait Islander communities.     

Bisphosphonates' use in metastatic bone disease

Bisphosphonates already have an established role in the management of the skeletal complications of metastatic bone disease. The development of new, highly potent compounds has led to investigation into their use as preventive agents in the adjuvant setting. The aim of the paper is to evaluate the evidence for their use in prevention and treatment.