Serum Phosphate Levels and Risk of Infection in Incident Dialysis Patients
Background and objectives: Hyperphosphatemia is highly prevalent in dialysis patients and may be associated with immune dysfunction. The association of serum phosphate level with infection remains largely unexamined.
Design, setting, participants, & measurements: In an incident cohort of 1010 dialysis patients enrolled from 1995 to 1998 and treated in 80 US clinics, the association of phosphate level (low <3.5; normal 3.5 to 5.5; high >5.5 mg/dl) at baseline and during follow-up with the risk for incident inpatient and outpatient infection-related events was examined. Infectious events were identified from US Renal Data System data (mean follow-up 3.3 yr). Incidence rate ratios for all infections, sepsis, respiratory tract infections, and osteomyelitis were obtained using multivariable Poisson models, adjusting for potential confounders (age, race, gender, smoking, comorbidity, and laboratory values).
Results: Infections of any type (n = 1398) were more frequent among patients with high phosphate levels at baseline, relative to normal; this association was not changed by adjustment for parathyroid hormone level. Similarly, high versus normal baseline phosphate was associated with increased risk for sepsis and osteomyelitis but not respiratory tract infections. Associations with calcium were generally NS, and results with calcium-phosphate product mirrored the phosphate results.
Conclusions: High phosphate levels may be associated with increased risk for infection, contributing further to the rationale for aggressive management of hyperphosphatemia in dialysis patients.
Effect of Tonsillectomy Plus Steroid Pulse Therapy on Clinical Remission of IgA Nephropathy: A Controlled Study
Background and objectives: Few well-designed investigations have examined how tonsillectomy plus steroid pulse therapy affects IgA nephropathy. A prospective, controlled study therefore was performed to compare the effects of combined therapy with those of steroid pulse alone in patients with IgA nephropathy.
Design, setting, participants, & measurements: Fifty-five patients were followed up for 54.0 ± 21.2 mo. Thirty-five of them underwent tonsillectomy and steroid pulse therapy (group C), and 20 received steroid pulse monotherapy (group M). Both groups received methylprednisolone intravenously, followed by oral prednisolone (initial dosage 0.5 mg/kg per d) for 12 to 18 mo. Primary evaluation items were a 100% increase in serum creatinine from baseline levels or the disappearance of urinary protein (UP) and/or occult blood (UOB) indicating clinical remission.
Results: At 24 mo after the initial treatment, the ratios of the UP and UOB disappearance were higher in group C than in group M, and the therapeutic effect persisted until the final observation. None of group C achieved a 100% increase in serum creatinine from the baseline level, whereas one patient in group M developed ESRD during the observation period. The histologic findings of repeated biopsy specimens from 18 patients revealed that mesangial proliferation and IgA deposition were significantly more reduced in group C than in group M. The Cox regression model showed that the combined therapy was approximately six-fold more effective in causing the disappearance of UP than steroid pulse monotherapy.
Conclusion: Tonsillectomy combined with steroid pulse treatment can induce clinical remission in patients with IgA nephropathy.
Pulmonary Hypertension, Right Ventricular Failure, and Kidney: Different from Left Ventricular Failure?
In this article, the pathophysiology of left ventricular failure is reviewed. By contrast, the paucity of information about pulmonary arterial hypertension and right ventricular failure is acknowledged. The potential mechanisms whereby renal sodium and water retention in right ventricular failure secondary to pulmonary arterial hypertension can occur, despite normal left ventricular function, are discussed. With right ventricular failure as the primary cause of death in patients with pulmonary hypertension, more information about the mechanisms of renal sodium and water retention in these patients is direly needed. Specifically, studies to examine the activation of the neurohumoral axis at various stages of pulmonary arterial hypertension and right ventricular failure, including inhibition of mineralocorticoid and V2 vasopressin receptors, are indicated.
Coronary Artery Calcification, ADMA, and Insulin Resistance in CKD Patients
Background and objectives: It is known that coronary artery calcification (CAC) develops in chronic kidney disease (CKD) before initiation of renal replacement therapy, and factors associated with CKD mineral and bone disorders (CKD-MBDs) are involved. However, little information is available about any association between plasma levels of asymmetric dimethylarginine (ADMA), insulin resistance, and CAC.
Design, setting, participants, & measurements: A total of 111 CKD patients (79 men, 32 women; glomerular filtration rate [GFR] median, 33.7 ml/min per 1.73 m2), free of cardiovascular disease, were consecutively recruited along with 30 age-matched healthy subjects. Coronary artery calcification scores (CACS) were measured by multidetector-row CT according to Agatston score.
Results: In CKD patients, CACS was distributed widely from 0 to 2901, while in age-matched, healthy control subjects (n = 30), CACS showed a range from 0 to 307. GFR had a significant negative correlation with CACS. Plasma ADMA levels were negatively correlated with GFR and positively correlated with CACS. When CACS was divided into quartiles (<50, n = 56; 50 to 300, n = 24; 300 to 600, n = 14; >600, n = 17), the patients with CACS >600 had significantly higher values of HOMA-IR, plasma ADMA levels, and fibrinogen along with serum levels of phosphorus, compared with those in patients having CACS <50. Multivariate regression analysis determined HOMA-IR as an independent contributing factor to CACS.
Conclusions: CAC becomes more prevalent and severe with a decline in GFR, and plasma ADMA levels and insulin resistance, independent of factors associated with CKD-MBD, are correlated with CAC.
