The KDIGO (Kidney Disease: Improving Global Outcomes) 2012 clinical practice guideline for the management of blood pressure (BP) in chronic kidney disease (CKD) provides the structural and evidence ...base for the Canadian Society of Nephrology (CSN) commentary on this guideline’s relevancy and application to the Canadian health care system. While in general agreement, we provide commentary on 13 of the 21 KDIGO guideline statements. Specifically, we agreed that nonpharmacological interventions should play a significant role in the management of hypertension in patients with CKD. We also agreed that the approach to the management of hypertension in elderly patients with CKD should be individualized and take into account comorbid conditions to avoid adverse outcomes from excessive BP lowering. In contrast to KDIGO, the CSN Work Group believes there is insufficient evidence to target a lower BP for nondiabetic CKD patients based on the presence and severity of albuminuria. The CSN Work Group concurs with the Canadian Hypertension Education Program (CHEP) recommendation of a target BP for all non–dialysis-dependent CKD patients without diabetes of ≤140 mm Hg systolic and ≤90 mm Hg diastolic. Similarly, it is our position that in diabetic patients with CKD and normal urinary albumin excretion, raising the threshold for treatment from <130 mm Hg systolic BP to <140 mm Hg systolic BP could increase stroke risk and the risk of worsening kidney disease. The CSN Work Group concurs with the CHEP and the Canadian Diabetic Association recommendation for diabetic patients with CKD with or without albuminuria to continue to be treated to a BP target similar to that of the overall diabetes population, aiming for BP levels < 130/80 mm Hg. Consistent with this, the CSN Work Group endorses a BP target of <130/80 mm Hg for diabetic patients with a kidney transplant. Finally, in the absence of evidence for a lower BP target, the CSN Work Group concurs with the CHEP recommendation to target BP < 140/90 mm Hg for nondiabetic patients with a kidney transplant.
Background Chronic kidney disease increases the risk of bone fragility fractures (osteoporotic fractures). Living kidney donors lose 50% of their renal mass and show changes in calcium homeostasis. ...We studied whether living kidney donation increases the risk of fragility fracture. Design Retrospective matched-cohort study. Setting & Participants We reviewed the medical charts of all 2,015 adults in Ontario, Canada, who donated a kidney between 1992 and 2009 (surgeries performed across 5 transplant programs). We linked this information to health care databases and randomly selected 20,150 matched nondonors from the healthiest portion of the general population. Median age was 43 (95% CI, 24-50) years at study enrollment. Donors and nondonors were then followed up for a median of 6.6 years and a maximum of 17.7 years. Predictor Living donor nephrectomy. Outcomes The primary outcome was lower- and upper-extremity fragility fractures. Individuals who reached 66 years or older in follow-up had bisphosphonate prescriptions recorded. Results The rate of fragility fracture was no higher in donors compared with nondonors (16.4 vs 18.7 events/10,000 person-years; rate ratio, 0.88; 95% CI, 0.58-1.32). Results were similar in multiple additional analyses. There was little difference in the proportion of older adults in follow-up who received a bisphosphonate prescription (17.1% vs 15.2%; P = 0.4). Limitations These are interim results. Ongoing surveillance of this and other donor cohorts is warranted to be sure an association does not manifest with longer follow-up. Conclusions To date, there is no evidence of increased fragility fracture risk in living kidney donors. Our results meet an information need and are reassuring for the safety of the practice.
Hyperuricemia is common after kidney transplantation. Although its risk factors are well established, its relation to inflammation, progressive renal dysfunction, and cardiovascular events is ...unknown. In this study, 405 stable renal transplant recipients with ≥3 uric acid (UA) and C-reactive protein measurements from January 2005 to April 2008 were identified to determine the relations between UA and C-reactive protein and between UA and the rate of decrease in the estimated glomerular filtration rate (eGFR; using the Modification of Diet in Renal Disease equation) and cardiovascular events. Hyperuricemia was defined as UA >7.1 mg/dl (420 μmol/L) in men and >6.1 mg/dl (360 μmol/L) in women. The prevalence of hyperuricemia was 44% (180 of 405). Hyperuricemia was negatively associated with eGFR (p <0.0001) and positively associated with diuretic use (p = 0.013), time since transplantation (p = 0.014), and triglycerides (p = 0.04). Although UA was correlated with C-reactive protein (p = 0.003), adjustment for eGFR rendered this relation nonsignificant (p = 0.225). The slope of eGFR was +0.144 ± 0.85 ml/min/1.73 m2 /month (95% confidence interval 0.032 to 0.257) in those with normal UA levels and −0.091 ± 0.93 ml/min/1.73 m2 /month (95% confidence interval −0.235 to +0.054) in patients with hyperuricemia (p = 0.003). There were 17 cardiovascular events in the patients with hyperuricemia and 4 in those with normal UA levels (p = 0.001). In conclusion, hyperuricemia is associated with a decrease in renal allograft function and may be an independent cardiovascular risk factor in transplant recipients. Further studies are needed to establish its role in post-transplantation cardiovascular disease.
