Nabil Haddad

Central Vein Stenosis: A Nephrologist's Perspective

Central vein stenosis is commonly associated with placement of central venous catheters and devices. Central vein stenosis can jeopardize the future of arteriovenous fistula and arteriovenous graft in the ipsilateral extremity. Occurrence of central vein stenosis in association with indwelling intravascular devices including short‐term, small‐diameter catheters such as peripherally inserted central catheters, long‐term hemodialysis catheters, as well as pacemaker wires, has been recognized for over two decades. Placement of multiple catheters, longer duration, location in subclavian vein, and placement on the left‐hand side of neck seem to predispose to the development of central vein stenosis. Endothelial injury with subsequent changes in the vessel wall results in development of microthrombi, smooth muscle proliferation, and central vein stenosis. Central vein stenosis is often asymptomatic in nondialysis patients, but can result in edema of ipsilateral extremity and breast when challenged by increased flow from an arteriovenous fistula or arteriovenous graft. Bilateral central vein stenosis or superior vena cava stenosis can produce a clinical picture of superior vena cava syndrome, associated with engorgement of face and neck. Endovascular interventions are the mainstay of management of central vein stenosis. Percutaneous angioplasty and stent placement for elastic and recurring lesions can restore the functionality of the vascular access, at least temporarily. Frequent or multiple interventions are usually required. In recalcitrant cases, surgical bypass of the obstruction is an option. In resistant cases with severe symptoms, occlusion of the functioning vascular access will usually provide relief of symptoms. Further study of mechanisms of development of central vein stenosis and search for a targeted therapy is likely to lead to better ways of managing central vein stenosis. Prevention of central vein stenosis is the key to avoid access failure and other complications from central vein stenosis and relies upon avoidance of central vein stenosis placement and timely placement of arteriovenous fistula in prospective dialysis patient.

D-Dimer Level and the Risk for Thrombosis in Systemic Lupus Erythematosus

BACKGROUND AND OBJECTIVES Patients who have systemic lupus erythematosus (SLE) and manifest antiphospholipid antibodies (APA) are at increased risk for thrombosis; however, it is difficult to predict who will clot. This study tested the hypothesis that peak D-dimer level measured routinely during follow-up identifies whether a hypercoagulable state is developing and, therefore, the patient is at increased risk for thrombosis. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS One hundred consecutive patients who had SLE with recurrent activity (71% renal SLE) and were evaluated for or enrolled in the Ohio SLE Study were studied. D-dimer testing was done annually and usually at SLE flare or other serious illness. When D-dimer was elevated, evaluation for thrombosis (large vessel, small vessel, or Libman-Sacks) was undertaken. Mean follow-up was 37.5 +/- 15 SD months. RESULTS Of those with peak D-dimer <0.5 microg/ml (n = 46), 0% thrombosed, 33% had APA. Of those with peak D-dimer 0.5 to 2.0 microg/ml (n = 19), 6% thrombosed, 44% had APA. Of those with peak D-dimer >2.0 microg/ml (n = 36), 42% thrombosed, 76% had APA. The most common causes of elevated D-dimer in the absence of demonstrable thrombosis were SLE flare and systemic infection. D-dimer levels were usually elevated for several months before thrombosis. CONCLUSIONS Patients with SLE and normal D-dimer levels are at low risk for thrombosis, irrespective of APA status. Those with persistent unexplained elevated D-dimer levels, particularly when >2.0 microg/ml, are at high risk for thrombosis.

Usual ACE Inhibitor Therapy in CKD Patients Is Associated with Lower Plasma Aldosterone Levels than Usual Angiotensin Receptor Blocker Therapy

Background: Attenuating aldosterone (ALDO) effects may be important in slowing kidney and cardiovascular disease progression. This study tested whether ACE inhibitor (I) therapy achieves lower plasma (p) ALDO levels than angiotensin receptor blocker (ARB) therapy when they are used under usual clinical conditions in chronic kidney disease (CKD) patients. Methods: Consecutive CKD patients (n = 123) were studied. They were clinically stable and receiving either ACEI (n = 77) or ARB (n = 46) (physician’s choice) for ≧3 months. Results: Mean pALDO in the ACEI cohort was 7.8 ± 5.7 (SD) ng/dl compared to 12.3 ± 9.8 ng/dl in the ARB cohort (p = 0.0018, normal ambulatory pALDO 9.4–33.8 ng/dl). The pALDO difference was not explained by differences in age, sex, race, body weight, diagnosis of diabetes; the use of β-blockers, calcium channel blockers or diuretic; systolic or diastolic blood pressure; plasma renin, serum creatinine, sodium, potassium, or bicarbonate levels; 24-hour urine potassium, sodium, urea or protein excretion; or ACEI or ARB dose. Conclusions: Mean pALDO is about 60% higher with ARB therapy than ACEI therapy when these drugs are customarily used in CKD patients. This difference could be clinically important with regard to kidney and cardiovascular protection.

Iatrogenic Graft to Vein Fistula (GVF) Formation Associated with Synthetic Arteriovenous Grafts

The prevalence of fistulous connection between arteriovenous graft (AVG) and an adjacent vein resulting in graft‐vein fistula (GVF) formation is not established. AVG venous outflow stenosis along with repeated and traumatic cannulation is likely major contributing factor of this complication. Detection and resolution of venous outflow stenosis may be the only needed intervention. We report a series of eight cases with GVF formation between AVG and adjacent veins. Awareness of this complication and intervention to relieve stenotic lesions may result in improved AVG survival.

Nutritional Management of Water, Sodium, Potassium, Chloride, and Magnesium in Kidney Disease and Kidney Failure

The kidney plays a central role in regulating water and electrolyte balance. It does so by adjusting renal excretion of these molecules in response to changes in intake or output. So, it should come as no surprise that, when the kidney is diseased, electrolyte and water balance can be abnormal. What is surprising is how well the impaired kidney is able to maintain water and electrolyte balance until virtually all kidney function has been lost. In this chapter we discuss water and electrolyte homeostasis and show how it is perturbed by chronic kidney disease (CKD). Also, we provide recommendations for water and electrolyte management in CKD. Chloride is considered together with sodium because, generally, nearly all chloride intake is the result of the intake of salt (sodium chloride, NaCl).

Bath Salts: A Newly Recognized Cause of Acute Kidney Injury

Bath salts are substance of abuse that are becoming more common and are difficult to recognize due to negative toxicology screening. Acute kidney injury due to bath salt use has not previously been described. We present the case of a previously healthy male who developed acute kidney injury and dialysis dependence after bath salt ingestion and insufflation. This was self-reported with negative toxicology screening. Clinical course was marked by severe hyperthermia, hyperkalemia, rhabdomyolysis, disseminated intravascular coagulation, oliguria, and sepsis. We discuss signs and symptoms, differential diagnoses, potential mechanisms of injury, management, and review of the literature related to bath salt toxicity.

Thrombocytopenia in ESRD Patients: Epidemiology, Mechanisms and Interventional Nephrology Perspective

A well‐functioning vascular access is essential for provision of life‐sustaining dialysis treatment in patients with end‐stage renal disease. Arteriovenous accesses are preferred form of vascular access. Although significant advances have been made in the field of dialysis access, arteriovenous access dysfunction remains the single most important cause of morbidity in ESRD patients. While thrombosis and stenosis of AV access are more frequently seen, hemorrhage from AV access can be life threatening with or without risk of permanent access loss. Aside from anticoagulation for comorbidities, qualitative and/or quantitative platelet abnormalities are often the predisposing factors. We describe an ESRD patient who developed new onset but severe thrombocytopenia due to metastatic small cell neuroendocrine carcinoma of lung. Given her persistent thrombocytopenia and presence of prolonged bleeding from the cannulation sites, a right internal jugular tunneled dialysis catheter was placed for continuation of maintenance dialysis. This review discusses the definition of thrombocytopenia, mechanisms of thrombocytopenia in patients with ESRD and with a special focus on implications of thrombocytopenia on dialysis access interventions. The review underscores the need for consensus with regard to cannulating AV access as well as guidelines specific to dialysis access‐related endovascular intervention in the setting of thrombocytopenia and other coagulation abnormalities.

Central Venous Catheters in Dialysis: The Good, the Bad and the Ugly

Central venous catheters (CVC) continue to remain a common modality of vascular access in end stage kidney disease patients maintained on hemodialysis. The increased morbidity and mortality associated with CVC, when compared to arteriovenous fistulas and grafts, is a serious health problem and a big challenge to the nephrology community. In this article we present the pros and cons of CVC, in addition to the different complications and excessive economical costs related to their use.

LEARNING FROM IMAGES Seroma Related to Prosthetic Arteriovenous Graft

Seroma is a complication unique to prosthetic arteriovenous graft (AVG), resulting as a consequence of transudation of sterile and clear serum, which is confined by a non-secretory fibrous pseudomembrane [1]. Although the precise etiology remains elusive, it is thought to be related to failure of the surrounding connective tissue to incorporate the graft [2]. The incidence of 2-4% reported in literature may not be a true representation due to frequently seen spontaneous resolution of seroma [2]. A seroma is typically located close to the arterial anastomosis and usually occurs within the first month after placement of the AVG [3] (Fig. 1). Ultrasound-guided needle aspiration of the fluid yielding serous or gelatinous material can be of both diagnostic and therapeutic significance. When in doubt, the fluid should be