NKF 2014 Spring Clinical Meetings Abstracts
317 COLLAPSING GLOMERULOPATHY AND AUTOIMMUNE DISORDERS- AN UNCLEAR ASSOCIATION: Nishkarsh Saxena, Kavitha Kesari, Susan Smith, Vaibhav Sahni, McLaren Hospital, Michigan State University, Flint, MI, USA Collapsing Glomerulopathy (CG) is an aggressive morphologic variant of focal segmental glomerulosclerosis (FSGS). CG is most commonly associated with HIV infection; rarely with other infections, autoimmune disorders, malignancies, drug exposures etc. We report a case of nephrotic syndrome secondary to CG with renal biopsy findings suggesting an underlying autoimmune disorder. A 27-year-old African American woman with no significant past medical history except multiple miscarriages and a family history of renal disease, presented with complaints of nausea, vomiting and generalized swelling. Her work up showed nephrotic range proteinuria (26 gm/d), acute kidney injury (Serum Creatinine 1.5-2.0 mg/dL) and severe hypoalbuminemia. Initial work up including Hepatitis Panel, HIV antibody, ANA titers, dsDNA, ASO, APLA titers and serum complement levels were normal. Renal biopsy revealed FSGS (collapsing variant); electron microscopy revealed electron dense mesangial deposits and immunofluoresence showed mesangial deposits (IgG, IgA and IgM, C1q, C3) without endocapillary deposits, making histology consistent with CG with immune deposits of unclear significance. She had a partial response to high dose oral steroids and tacrolimus. In spite of switching to mycophenolate mofetil, her renal function progressively declined. CG is characterized with severe proteinuria, progressively worsening renal function and poor therapeutic response. There are case reports suggesting an association between CG and SLE, with positive ANA and hypocomplementemia. Our patient is unique in having mesangial 'full house' spectrum immune deposits without clinico-serological or histological evidence of SLE or other autoimmune disorders. The pathogenesis and association of CG with autoimmune disorders and treatment in non-HIV patients remain elusive given its rarity.
318 REDUCTION IN ESA REQUIREMENT WITH ORAL ASCORBIC ACID IN HEMODIALYSIS PATIENTS WITH FUNCTIONAL IRON DEFICIENCY Saxena Anil Kumar, Chandra M. Jha, Ahmad Chaaban, Al-Madani K. Ayman, Samara Abouchacra, Dastoor D. Hormazdiar Several small studies have shown that the intravenous (IV) administration of ascorbic acid could play a promising role in the anemia management in HD patients. Present clinical study was designed to investigate the role of oral Ascorbic acid in correction of anemia in HD patients with low Transferrin Saturation (T. Sat), high Ferritin and raised CRP levels- a state of relative iron deficiency and inflammation). This prospective investigation was carried out in the Out - Patients HD Facility of Mafraq Hospital Abu Dhabi, UAE. Of 261 patients on long-term HD 79 were identified having anemia with high ferritin and high CRP during the study period (January 2011 to December 2012). Subjects were randomized into Two Groups: Group I: n =39 (Control, Standard Care) and, Group II: n =40 (ORAL Ascorbic acid, 1000 mg three times per week). All the adults (≥18 years) on HD with Hb ≤10 mg / dL, Serum Ferritin ≥ 500 and CRP ≥ 5.0 mg / mL) were included in the study. Subjects with acute blood loss, clinical infection and those having malignancy were excluded from the study. Baseline data: Age, Gender, Dialytic age (months), Hb (g/dL), S. Iron, Ferritin, Transferrin saturation (T. Sat), CRP, intact PTH levels, dose and duration of Darbipoietin treatment, proportions of diabetic and elderly subjects with the percentage of patients with permanent HD catheters. Serial estimations of Hb, T. Sat, Ferritin, CRP and weekly requirement of Darbipoietin - were performed and statistically compared between Group I and Group II at 12 weeks, 24 weeks, 36 weeks and 48 weeks from the baseline values. Darbipoietin dose (μg / Kg q 4 weeks) was significantly lower (p=0.03) in Ascorbic acid group (Group II) than in Control group (Group I), at 48 weeks. Significantly higher Mean Hb (p = <0.02) and T.Sat (p=<0.001) with significantly lower Ferritin P = 0.004) and CRP levels (p=0.03) were observed in Ascorbic acid group (Group II) than in Control group (Group I), at 48 weeks. Oral ascorbic acid reduces inflammation and possibly thus leading to reduction in the Darbipoietin requirement in patients with functional iron deficiency.
319 BLOOD PRESSURE AND RENAL FUNCTION AFTER RENAL DENERVATION: INSIGHTS FROM THE GLOBAL SYMPLICITY REGISTRY Markus Schlaich1, Luis Ruilope2, Roland Schmieder3, Giuseppe Mancia4, Felix Mahfoud5, Michael Böhm5 1 Baker IDI Heart and Diabetes Institute, Melbourne, Australia; 2 Hospital 12 de Octubre, Madrid, Spain; 3Universität ErlangenNürnberg, Erlangen, Germany; 4University of Milano-Bicocca, Monza, Italy; 5Universitätskliniken des Saarlandes, Homburg, Germany The Global SYMPLICITY Registry (GSR) is a post-market surveillance study designed to evaluate the safety and efficacy of renal denervation (RDN) in “real world patients” with hypertension and/or other diseases characterized by elevated sympathetic drive. GSR is an open-label prospective study performed at ~200 sites; ≥5,000 subjects will be enrolled and followed according to local practice for 5 years. A minimum of 10% randomly assigned sites will have 100% monitoring. In over 1,000 GSR subjects enrolled as of August 2013, 62% had systolic blood pressure (BP) ≥ 160 mm Hg (or ≥150 mm Hg if they had diabetes) despite treatment with ≥3 antihypertensive medications, including a diuretic. Of these subjects, 47% had diabetes, 29% had renal disease, and 8% had heart failure. Estimated glomerular filtration rate (eGFR) was 78.2 ± 25.4 mL/min/1.73m2 at baseline. Systolic BP decreased from a mean of 176.5 ± 18.3 at baseline to 154.1 ± 20.4 mm Hg at 6 months (n=313, p<.0001). The change in systolic BP does not appear to be related to baseline eGFR. RDN-related complications were adjudicated and included 1 dissection, 1 pseudoaneurysm, and 1 hematoma. There were 2 deaths and 1 renal failure, all deemed unrelated to the procedure. No renal artery stenosis related to the procedure was reported. In this “real world” patient population, subjects with systolic BP ≥ 160 mm Hg (or ≥150 mm Hg if they had diabetes) enrolled thus far in the GSR demonstrate a favorable safety profile with a substantial reduction in systolic BP. Complete 6 month follow-up data will be reported in April.
320 ACUTE KIDNEY INJURY FROM AN UNUSUAL POISON: Arjun Sekar, Subhash Paudel, Ashish Verma, Siva Padmanabhan Sivakumar, Saint Vincent Hospital, Worcester, MA, USA Naphthalene toxicity from mothball ingestion is an uncommon form of poisoning in USA. Most reported cases are of hemolytic anemia in children with G6PD deficiency. We present a case of an adult with non accidental, non suicidal naphthalene toxicity. A 56 year old African American male presented with 3 days of progressive dyspnea, fatigue and jaundice. It began after he chewed a few mothballs to treat his halitosis as suggested by a friend. Pertinent findings were a BP of 160/85, tachypnea with clear lungs, SpO2 85% on room air and icterus. Arterial blood gas on 100% non-rebreather mask revealed: ph-7.37, pCO2-34.8, pO2-50, bicarbonate- 20.5 & O2 saturation-85%. Labs revealed methemoglobin level of 9% (normal< 1.5%), leukocytosis, hemolytic anemia (hemoglobin 8.0, hematocrit25.4, reticulocyte count-5.7%, LDH-979, total bilirubin-16.1, indirect bilirubin-15.3) & creatinine of 1.45. Initial management included supplemental oxygen, blood transfusions and methemoglobin level monitoring. Methylene blue was held as serum methemoglobin levels were under 20g/dl. Hemolysis led to profound acute kidney injury with initial oliguria and creatinine increasing to 13. He had 1 session of hemodialysis for uremia after which the kidney function improved. Gradually, oxygen saturation, liver function, hemolysis and clinical course improved. Methemoglobin levels became undetectable in 3 days. On follow up 4 weeks later his creatinine and blood counts were normal, but G6PD levels were low. Naphthalene is metabolized into many reactive metabolites by cytochrome P450 and then excreted in the urine. Patients with G6PD deficiency are at higher risk due to low tolerance to oxidative stress. Intravascular hemolysis leads to anemia, hemoglobinuria & acute tubular necrosis. Oxidation of ferrous to ferric form results in methhemoglobinemia which shifts the oxyhemoglobin curve to the left and peripheral pulse oximetry is unreliable as hypoxia occurs at tissue level. Treatment is largely supportive. Methylene blue is a reducing agent that donates an electron to reduce methemoglobin and is recommended if methemoglobin levels are greater than 20 g/dl. Methylene blue, by itself can exacerbate hemolysis in G6PD deficient individuals like our patient and is therefore contraindicated in G6PD deficiency.
Am J Kidney Dis. 2014;63(5):A1-A121