The associations between orthostatic blood pressure changes and extracellular volume in hemodialysis patients.

INTRODUCTION: Extracellular volume (ECV) predicts mortality in hemodialysis patients, but it is difficult to assess clinically. Peridialytic blood pressure (BP) measurements can help ECV assessment. Orthostatic BP is routinely measured clinically, but its association with ECV is unknown. METHODS: In a cohort of hypertensive hemodialysis patients, we measured posthemodialysis ECV/weight with bioimpedance spectroscopy and analyzed its association with post-HD orthostatic BP measurements obtained during routine care. Using linear and logistic regression, the primary outcomes were orthostatic BP change and orthostatic hypotension (OH) defined by systolic BP decrease of at least 20 mmHg or diastolic decrease of at least 10 mmHg. Model 1 controlled for sex, age, and diabetes. Model 2 additionally controlled for ultrafiltration rate and antihypertensive medications. We conducted sensitivity analysis using OH definition of systolic BP decrease of at least 30 mmHg. FINDINGS: Among 57 participants, mean orthostatic systolic BP change was -7.30 (20) mmHg and mean ECV/weight was 0.24 (0.04) L/kg. Post-HD ECV/weight was not associated with orthostatic systolic BP change (ß = 8.2, p = 0.6). There were 16 participants with and 41 participants without OH. The ECV/weight did not differ between these groups (0.22 [0.04] vs. 0.24 [0.05] L/Kg, p = 0.09) and did not predict OH in logistic regression (OR 11, 4.04; 95% CI 0.2-671, 0.03-0.530 in the two models.) In a sensitivity analysis, ECV/weight was lower in the OH group (0.22 [0.03] vs. 0.25 [0.04] L/kg, p = 0.005), but this was accompanied by differences in sex and diabetes. Using logistic regression, there was no independent association between ECV/weight with OH. DISCUSSION: Orthostatic systolic BP change after HD completion is not a reliable indicator of posthemodialysis ECV. When considering other factors associated with orthostatic BP, ECV/weight is not independently associated with OH. Although transient postdialytic differences in intravascular volume may be associated with OH, posthemodialysis OH does not necessarily indicate ECV depletion.

Gadolinium and nephrogenic systemic fibrosis: have we overreacted?

Imaging is an increasingly important part of clinical medicine and contrast enhancement adds valuable diagnostic information. Prior to 2006 gadolinium based contrast agents (GBCA) were used in patients with kidney disease in an attempt to avoid the adverse consequences of iodinated contrast agents. The amount administered often exceeded the United States Food and Drug Administration (FDA)-recommended dosing. After the association between GBCA and nephrogenic systemic fibrosis (NSF) was reported, usage of GBCA was markedly reduced in patients with kidney disease. As a result, iodinated contrast was often used in place of GBCA. Recently, several studies showed that the risk of NSF using GBCA with increased thermodynamic and kinetic stability or increased relaxivity along with a restricted use policy has dramatically reduced NSF risk in patients with chronic kidney disease (CKD). We discuss the risks of GBCA and iodinated contrast use in different stages of CKD and suggest that in some situations GBCA use may pose less overall risk to the patient with advanced kidney disease.

Nephrogenic systemic fibrosis and the use of gadolinium-based contrast agents.

Nephrogenic systemic fibrosis (NSF) is a disease seen exclusively in patients with decreased renal function. The use of gadolinium-based contrast agents (GBCAs) has a strong association with NSF. Linear non-ionic GBCAs that are more prone to release free gadolinium are the more likely to cause NSF. The number of reported cases has increased recently, and there are currently nine pediatric cases, the patients ranging in age from 8 years to 19 years, and the oldest adult patient is 87 years of age. The most successful treatment is improvement of renal function with renal transplantation or with recovery of acute kidney injury. NSF can be severely debilitating and even fatal. Avoidance of a GBCA in patients at risk, or limitation of the dose in the patients who need gadolinium enhancement, is recommended.

Nephrogenic systemic fibrosis risk: is there a difference between gadolinium-based contrast agents?

Nephrogenic systemic fibrosis (NSF) is a disabling and potentially fatal disease that has been associated with gadolinium-based contrast (GBC) agents. There are five GBC agents approved for use in the United States and another four approved in Europe. The proposed cause of NSF is release of free Gd3+ into tissues in patients with decreased renal function. The number of associated cases and the potential to release free gadolinium is not equal between these agents. Gadodiamide has the largest number of reported cases of NSF followed by gadopentetate dimeglumine and gadoversetamide. The market share of these agents may contribute to the number of reported cases. The pharmokinetics of gadodiamide and gadoversetamide indicate that these two agents are more likely to release free Gd3+ than other GBC agents. Gadoteridol and gadoterate meglumine have a cyclic structure, making them less likely to release free Gd3+, and there is only a single reported case of NSF associated with gadoteridol use alone. Further research into individual agents is needed.

What nephrologists need to know about gadolinium.

Gadolinium chelates are commonly used to improve tissue contrast in MRI. Until recently the use of gadolinium was thought to be risk-free compared with alternative contrast agents. Recent studies, however, have raised serious concerns regarding the safety of gadolinium chelates. Although safe in patients with normal kidney function, administration of these agents in people with renal dysfunction can result in up to three clinical problems that the nephrologist should be familiar with. The first is nephrogenic systemic fibrosis (NSF), which was initially observed in 1997. Although manifesting primarily in skin, NSF can also cause systemic fibrosis, leading to disabling contractures and even death. Gadodiamide is the agent that has been most frequently associated with NSF, but other chelates might also pose a risk. The second clinical problem is that gadolinium chelates cause acute kidney injury, especially at high doses required for angiography. The third problem is that several laboratory artifacts are associated with gadolinium administration, with pseudohypocalcemia being the most important. The risk of a patient experiencing all three of these complications increases as renal function declines. In light of these problems, nephrologists need to re-evaluate the risks and benefits of gadolinium administration in patients with chronic kidney disease stage 3 or greater, as well as in those with acute kidney injury.

Multiple myeloma in end-stage renal disease.

Multiple myeloma is a common cause of chronic kidney disease (CKD). Patients with myeloma-related kidney disease but low levels of serum monoclonal proteins can be diagnosed with symptomatic myeloma in a simplified diagnostic classification. The presence and type of renal disease in myeloma is dependent on the light chain secreted. Treatment has recently changed and now includes the use of thalidomide and bisphosphonates. Thalidomide can cause hyperkalemia and bisphosphonates can cause renal failure in patients with CKD. Their use is not contraindicated, but they should be used with caution. High-dose melphalan with an autologous stem cell transplant is now the standard of care and should not be withheld from patients with CKD, even those on dialysis. This treatment can improve the renal disease, and this is more likely if treatment is started early. In patients with persistent dialysis dependence, renal transplantation can be performed if the patient has a complete remission.