Mineral Bone Disease Research Articles

Fibroblast Growth Factor 23 (FGF 23) and intact parathyroid hormone (iPTH) as markers of mineral bone disease among Nigerians with non-diabetic kidney disease.

Excess cardiovascular burden in patients with chronic kidney disease (CKD) has been attributed to the occurrence of CKD-Mineral Bone Disease (CKD - MBD). This study aimed to determine the spectrum of CKD-MBD among Nigerians with CKD using Fibroblast Growth Factor 23 (FGF 23) and intact Parathyroid Hormone (iPTH). Cross sectional survey of 105 patients with non-diabetic CKD and 104 controls. Information obtained were demographics, aetiology of CKD, features of CKD-MBD. Serum iPTH and FGF 23 were assayed. The mean ages were 48.7±15.3 vs 48.6±17.4 years while 54.7% and 45.2% were males for cases and controls, respectively. The mean plasma FGF 23 (392.8±35.3 vs 133.8±22.7 RU/mL and plasma iPTH (289±25.6 vs 118±10.8 ng/L, respectively. The frequency of elevated FGF 23 (45.7% vs 24.0%, p<0.01) and abnormal iPTH (53.3% vs 14.1%, p- 0.01) were higher in cases. The prevalence of MBD were (59.0% vs 14.4%, p<0.01) in cases and controls while dialysis status OR 2.94, 95% CI (1.2803-5.3645), and elevated FGF 23 OR, 1.87, 95% CI (1.1782-5.4291) were associated with CKD-MBD. The study demonstrated high prevalence of CKD-MBD among patients with non-diabetic CKD while FGF23 and iPTH were useful assays in the diagnosis of CKD-MBD among Nigerians with CKD.

POS-087 MINERAL BONE DISORDERS IN CHILDREN WITH SICKLE CELL ANEMIA AND ACUTE KIDNEY INJURY

Sickle cell anemia (SCA) is associated with an increased risk of bone complications that lead to significant long-term morbidity. Acute Kidney Injury (AKI) is a common complication of children with SCA vaso-occlusive crises (VOC) and may exacerbate bone disease. We evaluated the prevalence of sickle-cell related mineral bone disease (sMBD) in children with SCA hospitalized for a painful VOC based on the presence of AKI and other kidney abnormalities.

The Influence of Parathyroidectomy on Osteoporotic Fractures in Kidney Transplant Recipients: Results from a Retrospective Single-Center Trial.

Kidney transplant (KTx) recipients are a high-risk population for osteoporotic fractures. We herein aim to identify the role of pre-transplant parathyroidectomy (PTX) and other modifiable factors associated with osteoporotic fractures in KTx recipients. We conducted a retrospective study involving 711 adult patients (4608 patient-years) who were transplanted at our center between January 2007 and June 2015. Clinical data were extracted from patients’ electronic medical records. Different laboratory and clinical parameters for mineral bone disease (MBD) and osteoporosis, including medication, were evaluated. We chose fracture events unrelated to malignancies or adequate trauma as the primary endpoint. Osteoporotic fractures occurred in 47 (6.6%) patients (median 36.7 months, IQR 45.9) after KTx (fracture incidence of 10 per 1000 person-years). Prior to KTx, subtotal PTX was performed in 116 patients (16.3%, median time 4.2 years before KTx, IQR 5.0). Of the patients with fracture (n = 47), only one (2.2%) patient had previously undergone PTX. After adjusting for the known fracture risk factors MBD and osteoporosis, PTX remained a protective factor against fractures (HR 0.134, CI 0.018–0.991, p = 0.049). We observed a reduced risk for pathological fractures in KTx patients who underwent PTX, independent from elevated parathyroid hormone at the time of KTx or afterwards.

Outcome of Parathyroidectomy for Renal Hyperparathyroidism: A Single Center Experience

Background: Renal hyperparathyroidism (HPTH) is a common complication of chronic kidney disease and is known to cause significant morbidity in these patients. There has been substantial debate on the best possible treatment of this condition. Surgical treatment is now considered to be of vital importance as its efficacy is well documented. The present study reported the outcome of parathyroidectomy in King Chulalongkorn Memorial Hospital, a university hospital in Bangkok, Thailand. Objective: To determine surgical outcomes, including success rate and perioperative complications of parathyroidectomy in patients with renal HPTH. Materials and Methods: The data was collected by retrospective review of patients’ records between June 2014 and May 2019. One hundred ten patients were enrolled. Their demographic data, laboratory results, and outcomes were collected and categorized. Results: Among 110 patients, men accounted for 48.6%. The mean age was 49.5 years (SD 13.3). The most frequent operation was total parathyroidectomy with autotransplantation (TPTX+AT). All four glands were identified and excised in 84.5% of all patients. The mean preoperative serum intact parathyroid hormone (iPTH) level was 1,938 pg per dL with a range of 171 to 5,000 pg per dL. Postoperative hypocalcemia requiring intravenous calcium supplement was present in 70%. Postoperative cardiovascular complication occurrences were 16.4%, with one mortality due to myocardial infarction. In addition, one patient suffered unilateral recurrent laryngeal nerve injury, while two had stroke. The overall success rate of treatment was 81.1%, with 7.3% and 8.2% of patients that had persistently high PTH and recurrence of HPTH, respectively. Conclusion: Parathyroidectomy is an essential choice of treatment in patients with renal HPTH. Further validation of correlations with other factors is now being processed, and more data are needed. Keywords: Secondary hyperparathyroidism; Tertiary hyperparathyroidism; Chronic kidney disease mineral bone disease; Parathyroidectomy

Immune dysfunction in chronic kidney disease

Chronic kidney disease is characterized by immune dysfunction that increases predisposition to infections, virus-associated cancers and impaired response to vaccination. The altered immune response is caused by impairment of both innate and adaptive immune systems, as well as other factors that are hallmarks of renal disease, such as uremia, malnutrition, chronic inflammation, mineral bone disease and anemia. The aim of this article is to review the causes and mechanisms that lead to immune dysfunction in patients with chronic kidney disease.

The Relationship between Serum Osteopontin level and Parameters of Chronic Kidney Disease – Mineral Bone Disease in Patients on Regular Hemodialysis

The Relationship between Serum Osteopontin level and Parameters of Chronic Kidney Disease – Mineral Bone Disease in Patients on Regular Hemodialysis

Update on Pediatric Hemodialysis Adequacy.

The use of high reflux dialyzers to achieve a Kt/Vurea above 1.2 did not improve patient survival in most literature reports. After an electronic search in many sites, guidelines, systematic reviews, and review articles (cited references): We recommend (1) using the equilibrated double-pool, weekly rather than per session, Kt/Vurea, (2) Use of UF-dry weight to avoid V changes, (3) consider protein catabolic Rate (4) Use of double pool to avoid urea generation rebound effect. Beyond the urea model, other recommended parameters include the middle molecule clearance and patient clinical data as blood pressure control, normal ventricular morphology, and function, absence of anemia, bone mineral disease, vascular calcifications, good nutrition and growth, long-lasting vascular access, less intra-dialysis hypotension, fewer hospitalizations related to complications as infection, long-term patient survival with better life quality. All mentioned parameters are the good markers for adequate dialysis. Since (1) frequent short and (or) slow long dialysis sessions show better solute clearance and hemodynamic stability associated with better control of cardiovascular and bone disease, anemia, nutrition, and growth with better quality of life and survival. (2) The spare in the cost of the antihypertensive medications, erythroid-stimulating drugs, phosphate binders, and frequent hospitalization, compensates for the high dialysis cost. (3) The use of some advisable techniques can minimize access trauma; therefore, HD Model can be changeable according to each patient's clinical and biochemical follow-up dialysis adequacy progress pattern.

Clinical factors associated with severe hypophosphataemia after kidney transplant

BackgroundThe mechanism by which hypophosphataemia develops following kidney transplantation remains debated, and limited research is available regarding risk factors. This study aimed to assess the association between recipient and donor variables, and the severity of post-transplantation hypophosphataemia.MethodsWe performed a single-centre retrospective observational study. We assessed the association between demographic, clinical and biochemical variables and the development of hypophosphataemia. We used linear regression analysis to assess association between these variables and phosphate nadir.Results87.6% of patients developed hypophosphataemia. Patients developing hypophosphataemia were younger, had a shorter time on renal replacement therapy, were less likely to have had a parathyroidectomy or to experience delayed graft function, were more likely to have received a living donor transplant, from a younger donor. They had higher pre-transplantation calcium levels, and lower alkaline phosphatase levels.Receipt of a living donor transplant, lower donor age, not having had a parathyroidectomy, receiving a transplant during the era of tacrolimus-based immunosuppression, not having delayed graft function, higher pre-transplantation calcium, and higher pre-transplantation phosphate were associated with lower phosphate nadir by multiple linear regression.ConclusionsThis analysis demonstrates an association between variables relating to better graft function and hypophosphataemia. The links with biochemical measures of mineral-bone disease remain less clear.

Single peritoneal dialysis centre observations of treatment adequacy, anemia treatment, inflammation, mineral bone disease, and peritonitis rate – In patients undergoing continuous ambulatory peritoneal dialysis versus automated peritoneal dialysis

Purpose: Peritoneal dialysis was introduced to our centre in 1998. The aim of our retrospective analysis was to evaluate the difference in treatment adequacy, erythropoietin requirements, serum haemoglobin, serum C–reactive protein (CRP) and serum intact parathyroid hormone (i–PTH) levels, and episodes of peritonitis in patients switching from continuous ambulatory peritoneal dialysis (CAPD) to automated peritoneal dialysis (APD). We introduce peritoneal dialysis as a method of treatment for end–stage renal disease and the results of a retros-pective analysis.&#x0D; Methods: From May 1998 to December 2013, we retrospectively reviewed 12 patients (9 males and 3 females; mean age, 52.8±11.7 years) who switched from CAPD to APD. According to the peritoneal equilibration test, 75% of the patients were high transporters. We compared thetwo periods regarding peritoneal treatment adequacy number (Kt/V), erythropoietin requirements, serum haemoglobin, and CRP and i–PTH levels. We analysed the episodes of peritonitis during the CAPD and APD periods.&#x0D; Results: The average time spent on CAPD was 747.1±1028.2 days, and the average time spent on APD was 1300.0±1042.0 days. For the CAPD period, the mean Kt/V was 2.13±0.43, the mean haemoglobin value was 117.8±6.2 g/l, the mean erythropoietin requirement was 5290.1±4641.4 IU/week, the mean CRP value was 8.7±9.3 mg/l, and the mean i–PTH value was 580.2±445.9 pg/ml. For the APD period, the mean Kt/V was 2.24±0.35, the mean haemoglobin value was 117.1±8.6 g/l, the mean erythropoietin requirement was 4829.9±4976.6 IU/week, the mean CRP value was 9.1±8.3 mg/l, and the mean i–PTH value was 550.5±400.0 pg/ml. When comparing the two treatment modalities with a paired samples test, we found no significant differences regarding time spent (p=0.273), Kt/V (p=0.159), haemoglobin concentration (p=0.804), erythropoietin requirements (p=0.303), and CRP (p=0.886) and i–PTH levels (p=0.802). Further, no difference in the rate of peritonitis episodes between both modalities was found.&#x0D; Conclusion: Both peritoneal dialysis modalities are equal with respect to treatment adequacy, erythropoietin requirements, serum haemoglobin concentration, CRP and i–PTH levels, and peritonitis episodes.

Toxic Effects of Indoxyl Sulfate on Osteoclastogenesis and Osteoblastogenesis.

Uremic toxins, such as indoxyl sulfate (IS) and kynurenine, accumulate in the blood in the event of kidney failure and contribute to further bone damage. To maintain the homeostasis of the skeletal system, bone remodeling is a persistent process of bone formation and bone resorption that depends on a dynamic balance of osteoblasts and osteoclasts. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates the toxic effects of uremic toxins. IS is an endogenous AhR ligand and is metabolized from tryptophan. In osteoclastogenesis, IS affects the expression of the osteoclast precursor nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) through AhR signaling. It is possible to increase osteoclast differentiation with short-term and low-dose IS exposure and to decrease differentiation with long-term and/or high-dose IS exposure. Coincidentally, during osteoblastogenesis, through the AhR signaling pathway, IS inhibits the phosphorylation of ERK, and p38 reduces the expression of the transcription factor 2 (Runx2), disturbing osteoblastogenesis. The AhR antagonist resveratrol has a protective effect on the IS/AhR pathway. Therefore, it is necessary to understand the multifaceted role of AhR in CKD, as knowledge of these transcription signals could provide a safe and effective method to prevent and treat CKD mineral bone disease.

Clinical and scanographic mandibular abnormalities in patients with secondary hyperparathyroidism on maintenance hemodialysis

BackgroundMineral bone diseases in dialysis patients is a common but disturbing phenomenon. The involvement of the mandibular bone has been noted but few studies have investigated this in the sub Saharan region. ObjectifTo describe the clinical and scanographic mandibular abnormalities in patients with secondary hyperparathyroidism on maintenance haemodialysis. MethodWe conducted a cross sectional study where we included patients who had been on maintenance haemodialysis for at least 4 months with biochemical evidence of secondary hyperparathyroidism. We collected relevant medical and oral history. Thereafter, we evaluated oral functional status and performed CT scans of the mandible. Mandibular abnormalities, mental and gonial indices were noted. Data analysis was done with IBM SPSS 26.0 software. Statistical significance was set at a p value < 0.05. ResultsA total of 38 patients were enrolled with a mean ± SD age of 44 ± 12.9 years. The median PTH level and dialysis vintage were 807.6[605.0, 1166.0]pg/ml and 51.0 [51.3–92.8]months respectively. Twenty-nine (76.3%) participants had oral functional abnormalities with xerostomia (96.6%) and pain during mastication (62.1%) being the most frequent. Mental index was reduced in 96.7% of participants. Scanographic mandibular abnormalities were present in 94.7% of the participants with osteoporosis (100%) and alterations of the bone trabeculae (22.2%), the most prevalent. There was a negative correlation between the left (r = −0.405, p = 0.012) and right (r = −0.358, p = 0.027) gonion indices, the left (r = −0.358, p = 0.027), and right (r = −0.397, p = 0.014) mental indices and the PTH Level. PTH levels were significantly higher in mandibular cortical index Class C patients (p = 0.001). ConclusionMandibular involvement in mineral bone disease and oral function abnormalities were frequent.

Metabolic Acidosis and Cardiovascular Function in Chronic Kidney Disease

Metabolic acidosis (MA) is a very common finding in chronic kidney disease (CKD) and in cardiovascular disease due to the close relationship between the two organ systems. It depresses the myocardium; induces CKD; depresses urine acidification, bone mineral disease (CKD-BMD); and its presence reduces the quality of life, as well as increases cardiovascular events and mortality. The diagnostic strategies, patient assessment, treatment, prognostication, and possible patient referral entail good clinical acumen to prevent or limit complications, some of which can be fatal. Chronic metabolic acidosis in CKD is often associated with structural cardiac changes such as increased left ventricular mass and significant intradialysis blood pressure variations. The use of sevelamer, and the inhibitors of aldosterone in these patients could worsen MA; however, bicarbonate in the lower, upper normal, and elevated levels and its replacement could all be associated with various structural and functional cardiovascular changes.

The Combined Prognostic Significance of Alkaline Phosphatase and Intracranial Arterial Calcifications in Hemodialysis Patients

Introduction: The prevalence of intracranial arterial calcification (ICAC) in maintenance hemodialysis (MHD) patients is about 90%, and its severity is correlated with age, hemodialysis vintage, and mineral bone disease. Elevated concentrations of calcium and phosphorus are not sufficient for medial calcification because of inhibition by pyrophosphate. Alkaline phosphatase (ALP) promotes calcification by hydrolyzing extracellular pyrophosphate. Epigenetic mechanisms involving ALP inhibition by apabetalone were investigated as a potential target for preventing vascular calcifications (VCs). This study assessed the combined impact of VCs and elevated serum ALP on mortality among chronic HD patients. Methods: VCs represented by ICAC were measured simultaneously with mineral bone disease parameters including serum ALP of MHD patients who underwent noncontrast brain computed tomography from 2015 to 2018 in our institution. Results: This retrospective study included 150 MHD patients (mean age 71.3 ± 12.1 years, 60.1% male). Of the total cohort, 12 (7.8%) had no brain calcifications and 69 (45.1%) had multiple intracranial calcifications. Considering the patients with normal ALP and no calcification as the reference group yielded adjusted odds ratios for all-cause mortality of 4.6 (95% CI: 1.7–12.7) among patients with brain calcifications and normal ALP (p = 0.003) and odds ratios for all-cause mortality of 6.1 (95% CI: 2.1–17.7) among patients with brain calcifications and elevated ALP (p= 0.001). Conclusion: We found an independent association between ICAC and the risk of death among MHD patients. The combined effect of ICAC and elevated ALP was associated with a higher odds ratio for all-cause mortality in MHD patients and may contribute to the risk stratification of these patients.

Update on imaging in chronic kidney disease-mineral and bone disorder: promising role of functional imaging.

Disorders of mineral metabolism and bone disease are common complications in chronic kidney disease (CKD) patients and are associated with increased morbidity and mortality. Bone biopsies, bone scintigraphy, biochemical markers, and plain films have been used to assess bone disorders and bone turnover. Of these, functional imaging is less invasive than bone/marrow sampling, more specific than serum markers and is therefore ideally placed to assess total skeletal metabolism. 18F-sodium fluoride (NaF) PET/CT is an excellent bone-seeking agent superior to conventional bone scan in CKD patients due to its high bone uptake, rapid single-pass extraction, and minimal binding to serum proteins. Due to these properties, 18F-NaF can better assess the skeletal metabolism on primary diagnosis and following treatment in CKD patients. With the increased accessibility of PET scanners, it is likely that PET scanning with bone-specific tracers such as 18F-NaF will be used more regularly for clinical assessment and quantitation of bone kinetics. This article describes the pattern of scintigraphic/functional appearances secondary to musculoskeletal alterations that might occur in patients with CKD.

Effects of romosozumab or denosumab treatment on the bone mineral density and disease activity for 6 months in patients with rheumatoid arthritis with severe osteoporosis: An open-label, randomized, pilot study

ObjectivesTo investigate effects of romosozumab treatment on disease activity and bone mineral density (BMD) in patients with rheumatoid arthritis (RA) and severe osteoporosis in comparison with effects of denosumab treatment. MethodsA total of 50 women were enrolled in this study. The subjects were randomized equally into 2 groups: the romosozumab group or the denosumab group. Disease activity score in 28 joints (DAS28)-erythrocyte sedimentation rate (ESR) and BMD at lumbar spine were evaluated. ResultsThe percent changes (Δ) in the BMD values at 3 and 6 months for the lumbar spine were as follows: romosozumab; 4.9% and 5.2%, denosumab: 2.3% and 3.2%. The ΔBMD for the lumbar spine at 3 months was significantly higher in the romosozumab group than in the denosumab group (P = 0.044). The DAS28-ESR at baseline, 3 and 6 months in the romosozumab group were 2.88, 2.60 (P = 0.427) and 2.58 (P = 0.588), respectively. The change from baseline in DAS28-ESR did not differ significantly between these 2 groups at any time point. ConclusionsThe present study revealed that romosozumab treatment is more effective than denosumab treatment in increasing BMD of the lumbar spine at 3 months. Furthermore, the present study suggested that romosozumab treatment has no effects on the disease activity of RA in patients with RA and severe osteoporosis for 6 months.

Chronic Kidney Failure and Dialysis

Chronic kidney disease (CKD) is a clinical syndrome arising from progressive kidney injury, formerly known as chronic renal failure, chronic renal disease, and chronic renal insufficiency. It is classified into five stages based primarily on glomerular filtration rate (GFR). This article discusses the epidemiology of CKD and end-stage renal disease (ESRD), as well as etiology and genetics, pathophysiology, and pathogenesis. The section on diagnosis looks at clinical manifestations and physical findings, laboratory (and other) tests, imaging studies, and biopsy. A short section on differential diagnosis is followed by a discussion of treatment, including hemodialysis and peritoneal dialysis. Long-term complications of patients on dialysis include cardiovascular disease, renal osteodystrophy, dialysis-related amyloidosis, and acquired cystic disease (renal cell carcinoma). The final section addresses prognosis and socioeconomic burden. Figures include the classification system for CKD, prevalence of CKD in the United States, rising prevalence, risk of, and leading causes of ESRD in the United States, plus the changing prevalence of ESRD over time, clinical manifestations of uremia, and an overview of hemodialysis circuit. Tables look at the burden of CKD relative to other chronic disorders, the specific hereditary causes of kidney disease, and situations when serum creatinine does not accurately predict GFR. Other tables list equations for estimating GFR, the causes of CKD without shrunken kidneys, and clinical features distinguishing chronic kidney disease from acute kidney injury. ESRD and indications for initiation of dialysis are presented, as well as typical composition of dialysate and reasons for failure of peritoneal dialysis. This chapter contains 8 figures, 17 tables and 77 references Keywords: Renal disease, chronic kidney disease, hemodialysis, peritoneal dialysis, end-stage renal disease, glomerular filtration rate, mineral bone disease

Chronic Kidney Failure and Dialysis

Chronic kidney disease (CKD) is a clinical syndrome arising from progressive kidney injury, formerly known as chronic renal failure, chronic renal disease, and chronic renal insufficiency. It is classified into five stages based primarily on glomerular filtration rate (GFR). This article discusses the epidemiology of CKD and end-stage renal disease (ESRD), as well as etiology and genetics, pathophysiology, and pathogenesis. The section on diagnosis looks at clinical manifestations and physical findings, laboratory (and other) tests, imaging studies, and biopsy. A short section on differential diagnosis is followed by a discussion of treatment, including hemodialysis and peritoneal dialysis. Long-term complications of patients on dialysis include cardiovascular disease, renal osteodystrophy, dialysis-related amyloidosis, and acquired cystic disease (renal cell carcinoma). The final section addresses prognosis and socioeconomic burden. Figures include the classification system for CKD, prevalence of CKD in the United States, rising prevalence, risk of, and leading causes of ESRD in the United States, plus the changing prevalence of ESRD over time, clinical manifestations of uremia, and an overview of hemodialysis circuit. Tables look at the burden of CKD relative to other chronic disorders, the specific hereditary causes of kidney disease, and situations when serum creatinine does not accurately predict GFR. Other tables list equations for estimating GFR, the causes of CKD without shrunken kidneys, and clinical features distinguishing chronic kidney disease from acute kidney injury. ESRD and indications for initiation of dialysis are presented, as well as typical composition of dialysate and reasons for failure of peritoneal dialysis. This chapter contains 8 figures, 17 tables and 77 references Keywords: Renal disease, chronic kidney disease, hemodialysis, peritoneal dialysis, end-stage renal disease, glomerular filtration rate, mineral bone disease

Association of fibroblast growth factor-23 among chronic kidney disease patients with mineral bone disease

Background: Chronic kidney disease (CKD) is characterized by slow and progressive loss of kidney function over years. Most of the time it goes undetected till severe irreparable damage has occurred. CKD is a worldwide public health problem.Methods: The present cross sectional study was conducted in nephrology outpatient department (OPD) and medicine wards of Government Medical College and Hospital, Ambikapur, Sarguja, Chhattisgarh, India from June 2020 to June 2021. The study involved 50 adult patients (&gt;18 years) of CKD who were on hemodialysis. Patients who are not willing to participate and comatose patients were excluded from the study.Results: Among the CKD patients, 10 (20%) had left ventricular hypertrophy, 5 (10%) patients had left ventricular dysfunction with ejection fraction (EF) less than 40. 98% of the study participants were undergoing twice weekly hemodialysis and 2% were on thrice weekly hemodialysis. No significant association was found between left ventricular hypertrophy (LVH), pulmonary arterial hypertension (PAH), left ventricular dysfunction (LVD) with fibroblast growth factor-23 (FGF-23) (p&gt;0.05) whereas there was a significant association between phosphate and FGF-23 (p&lt;0.05) and between calcium and FGF-23 (p&lt;0.05).Conclusions: CKD mineral and bone metabolism (MBD) is common in patients with CKD especially stage 5. They are also prone for cardiovascular manifestation. FGF23 levels were high in those with elevated phosphorous, left ventricular hypertrophy and left ventricular dysfunction. Levels of calcium, intact parathyroid hormone (iPTH) and ejection fraction did not correlate with FGF-23. Larger population in the study would have helped in actual identification of these patients and also helped in the knowing the predominant role of FGF-23.

A Comparison of Hemodialysis and Peritoneal Dialysis in Patients with Cardiovascular Disease.

The high prevalence of cardiovascular disease is caused by the traditional cardiovascular risk factors common among end-stage renal disease patients, and nontraditional risk factors attributed to underlying kidney disease, including chronic inflammation, anemia, bone mineral disease, and the dialysis procedure itself. Individualization of the treatment of cardiovascular disease in end-stage renal disease that could impact the underlying mechanisms of the cardiovascular diseases is important to improve outcomes. This article reviews and compares hemodialysis and peritoneal dialysis in association with different cardiovascular diseases affecting dialysis patients, including hypertension, coronary artery disease, myocardial stunning, cardiac arrhythmias, heart failure, and the cardiorenal syndrome.

A Case of Fluorosis: Fluoride-Induced Osteopetrosis

There are multiple etiologies of increased bone density, including osteopetrosis and fluorosis. Osteopetrosis can either be a malignant autosomal recessive condition found in children or a benign autosomal dominant adult variant; both of which are characterized by decreased bone resorption. In contrast, fluorosis is characterized by increased bone formation secondary to chronic fluoride intoxication, but with a similar clinical manifestations to osteopetrosis.A 70-year-old lady with generalized joint aches, stiffness as well as fatigue, was found to have high bone mineral density and alarmingly high fluoride levels. The patient was found to be drinking fluoride containing water from an untreated local well for many years.Fluorosis results in increased bone mineral density and disease progression correlates with length of exposure. Fluorosis can result in reversible musculocutaneous symptoms and radiological findings. However, severe chronic cases may develop irreversible neurologic manifestations. Urinary fluoride testing is the screening modality of choice, and the key component of management is avoidance of the source of fluoride intoxication as well as monitoring of urinary fluoride levels.