An indolent cause of high-output heart failure in end-stage kidney disease-Application of the Nicoladoni-Israel-Branham test: A case report.

BACKGROUND: A hemodynamically significant arteriovenous fistula (AVF) in end-stage kidney disease (ESKD) causes a high flow state, resulting in pathologic cardiovascular remodeling, and deserves timely clinical recognition. CASE: A 55-year-old woman with history of ESKD with deceased donor kidney transplant with failing graft function and baseline creatinine of 2.8 mg/dl presented to the clinic with nocturnal cough, orthopnea, dyspnea on exertion and pedal edema. Physical exam was notable for large, aneurysmal right brachial AVF. Transthoracic echocardiography (TTE) revealed left ventricular (LV) enlargement and hypertrophy and elevated cardiac output (CO) of 10 L/min, raising a clinical concern for high-output heart failure. DECISION MAKING: A non-invasive assessment of the hemodynamic significance of the AVF was performed using a TTE. During temporary occlusion of the AVF, it was determined that about 27% of the resting CO was attributed to the AVF, suggesting hemodynamic significance. Nicoladoni-Israel-Branham sign was negative as there was no change in patient's heart rate, but this was potentially attributed to beta-blockade and chronic loading conditions. She underwent AVF banding and 2-month later her presenting symptoms resolved, and a TTE showed a decrease in resting CO of 7.6 L/min with normalization of LV size. CONCLUSION: This case highlights several teaching points. Firstly, in patients with ESKD, a large AVF can contribute to a high CO state resulting in maladaptive cardiovascular remodeling. Secondly, TTE evaluation of the hemodynamic contribution of an AVF can be performed with the application of the Nicoladoni-Israel-Branham sign. Finally, some experts recommend pre-emptive banding or ligation of AVF after successful kidney transplantation as this has been shown to have symptomatic and cardiovascular benefits.

Hypertension after kidney transplantation.

BACKGROUND: Few studies have examined the possible role of blood pressure (BP), independent of acute rejection and graft function, on outcomes after kidney transplantation. METHODS: We investigated the prevalence, treatment, control, and clinical correlates of hypertension and its association with outcomes, using multivariate analyses with time-dependent covariates, in a retrospective cohort of 1,666 kidney transplant recipients. RESULTS: Hypertension was common, and its control was poor. For example, at 1 year, only 55.5% had a BP less than 140 mm Hg. Control improved only slightly in 1993-2002 compared to 1976-2002, even as patients administered 2 or more antihypertensive medications at 1 year increased from 43.5% to 54.6%. Independent correlates of higher BP included male sex, age, donor age, diabetes, body mass index, the presence of native kidneys, and delayed graft function. Previous acute rejection was associated with higher BP at virtually all times after transplantation, and these associations were independent of estimated creatinine clearance (C(Cr)). Conversely, an association between BP and subsequent acute rejection was not statistically significant when differences in C(Cr) were taken into account. After adjusting for the effects of acute rejection, C(Cr), and other variables, each 10 mm Hg of systolic BP was associated with an increased relative risk for graft failure (1.12; 95% confidence interval, 1.08 to 1.15; P < 0.0001), death-censored graft failure (1.17; 1.12 to 1.22; P < 0.0001), and death (1.18; 1.12 to 1.23; P < 0.0001). CONCLUSION: High BP is closely tied to graft function, but nevertheless is an independent risk factor for graft failure and mortality. Better strategies are needed to control BP after kidney transplantation.

Hyperlipidemia in kidney disease: causes and consequences.

Dyslipidemias are common in patients with chronic kidney disease. The causes vary with the stage of kidney disease, the degree of proteinuria, and the modality of end-stage renal disease treatment. Dyslipidemias have been associated with kidney disease progression, and a number of small, randomized, controlled trials of lipid-lowering agents have been conducted. Unfortunately, the results of these trials, although encouraging, have been inconclusive because of the small numbers of patients enrolled. Dyslipidemias may also contribute to the high incidence of cardiovascular disease in patients with chronic kidney disease. This is most likely for patients with chronic renal insufficiency and for kidney transplant recipients. Less certain is the role of dyslipidemias in the pathogenesis of cardiovascular disease among dialysis patients.