Acute Kidney Injury in Subjects With Chronic Kidney Disease Undergoing Total Joint Arthroplasty.

BACKGROUND: Chronic kidney disease (CKD) has been associated with higher incidence of complications after total joint arthroplasty (TJA) but the incidence, risk factors and outcomes of acute kidney injury (AKI) in this setting remains insufficiently understood. METHODS: We assessed the impact of baseline CKD on the risk of developing AKI after TJA performed between 1/2012 and 12/2016 in a single-center, retrospective cohort study. CKD was defined by estimated glomerular filtration rate <60 mL/min/1.73 m2 on 2 separate occasions within 3 months prior TJA. AKI was defined using a modified Kidney Disease: Improving Global Outcomes criteria based on serum creatinine (sCr) only to assess the severity of AKI. Complete AKI recovery was defined as the lowest post-AKI sCr within 20% of pre-AKI sCr values and partial recovery if within 30%, all within 90 days after TJA. RESULTS: Twenty-four percent of the 1,212 subjects undergoing TJA had pre-existing CKD. The overall incidence of AKI in the CKD subjects was 30%; of these, 55% had stage-1 AKI, 1% had stage-2 AKI and 44% had stage-3 AKI. AKI was more common in African Americans, those with diabetes or heart failure, requiring perioperative transfusions or receiving diuretics before surgery. While 82% of the AKI subjects achieved complete recovery of kidney function, 4% had only partial recovery and 14% did not reach a post-AKI sCr level within 30% of pre-AKI values. The incidence (P < 0.001) but not the severity (P = 0.202) of AKI correlated with stages of baseline CKD. CONCLUSIONS: The presence of CKD was associated with a high incidence of AKI after TJA. In these subjects, more than half the cases of AKI were of mild degree and had a favorable outcome. However, 18% of them did not have complete recovery of kidney function. Stages of baseline CKD were associated with increased incidence but not severity of AKI after TJA.

Orthostatic changes in systolic blood pressure among SPRINT participants at baseline.

Orthostatic changes in systolic blood pressure (SBP) impact cardiovascular outcomes. In this study, we aimed to determine the pattern of orthostatic systolic pressure changes in participants enrolled in the SBP Intervention Trial (SPRINT) at their baseline visit before randomization and sought to understand clinical factors predictive of these changes. Of the 9323 participants enrolled in SPRINT, 8662 had complete data for these analyses. The SBP after 1 minute of standing was subtracted from the mean value of the three preceding seated SBP values. At the baseline visit, medical history, medications, anthropometric measures, and standard laboratory testing were undertaken. The mean age of SPRINT participants was 68 years, two-thirds were male, with 30% black, 11% Hispanic, and 55% Caucasian. The spectrum of SBP changes on standing demonstrated that increases in SBP were as common as declines, and about 5% of participants had an increase, and 5% had a decrease of >20 mm Hg in SBP upon standing. Female sex, taller height, more advanced kidney disease, current smoking, and several drug classes were associated with larger declines in BP upon standing, while black race, higher blood levels of glucose and sodium, and heavier weight were associated with more positive values of the change in BP upon standing. Our cross-sectional results show a significant spectrum of orthostatic SBP changes, reflecting known (eg, age) and less well-known (eg, kidney function) relationships that may be important considerations in determining the optimal target blood pressure in long-term outcomes of older hypertensive patients.

Characterization and treatment of resistant hypertension.

Resistant hypertension is a common medical problem. It carries a significantly increased risk of end-organ damage and cardiovascular events compared with more easily controlled hypertension. Resistant hypertension is most often related to isolated systolic hypertension and is characterized by aldosterone excess and increased intravascular volume. Its diagnosis requires the exclusion of pseudoresistance. The etiology of resistant hypertension is almost always multifactorial. Common reversible contributing factors need to be identified and addressed. Secondary causes of hypertension, such as primary aldosteronism, parenchymal and vascular kidney disease, and obstructive sleep apnea, require investigation and effective treatment if present. Therapy for resistant hypertension should be based on use of rational drug class combinations at optimal doses, with particular attention to adequate diuretic use. The addition of an aldosterone antagonist may further improve blood pressure control.