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Isolated Renal Thrombotic Microangiopathy As an Initial Presentation of Scleroderma Without Other Systemic Manifestations of the Disease

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Isolated Renal Thrombotic Microangiopathy As an Initial Presentation of Scleroderma Without Other Systemic Manifestations of the Disease ISOLATED RENAL THROMBOTIC MICROANGIOPATHY AS AN INITIAL PRESENTATION OF SCLERODERMA WITHOUT OTHER SYSTEMIC MANIFESTATIONS OF THE DISEASE. Sri Ranga Bonam, Sirisha Chalasani, Sashidhar Bollini, Robert Grunberg, Richard Snyder The thrombotic microangiopathies (TMA) share a common pathway of vascular endothelial injury and thrombus formation. Scleroderma is an autoimmune disease and histologically, scleroderma renal crisis (SRC) is indistinguishable from a TMA. To our knowledge, there are only several cases describing an association between the two. In those cases, patients with a TMA initially presented with either limited or diffuse scleroderma. We believe that this is the first time that an association between a TMA and scleroderma has been described in a patient without a pre-existing laboratory or clinical diagnoses of scleroderma. A 70 year old white male with past medical history significant only for hypertension and coronary artery disease presented with acute kidney injury (AKI). The patient was normotensive at this time, and prior had normal renal function. Serologic evaluation for connective tissue diseases was non-diagnostic. A renal biopsy demonstrated a TMA. The patient had no thrombocytopenia and no antiphospholipid antibodies. Because of the diagnostic dilemma concerning the etiology of the TMA, plasmapheresis and hemodialysis(HD) was started. The patient was transferred to a tertiary center where a repeat diagnostic evaluation was inconclusive. The patient was maintained on HD, and after a period of four months developed skin changes consistent with scleroderma. While the ANA was only mildly positive, and antibodies specific for scleroderma were negative. A skin biopsy demonstrated scleroderma-type changes. The skin manifestations quickly worsened, and the patient was started on D-Penicillamine and continued on HD. This case represents a rare presentation of a TMA that we think may have been a SRC with delayed onset of generalized scleroderma. A vWf cleaving protease assay may have helped in distinguishing between the SRC and TMA, as the treatment of each is different. If this was a SRC, it is also unusual that it preceded the skin manifestations. While not a leading diagnosis, scleroderma should be considered in the differential diagnosis of a TMA with AKI. ACUTE TUBULAR NECROSIS DUE TO OXALIPLATIN Manjeera Cherukuri, Richard Snyder, Rajen Oza, Easton Hospital/Drexel University College of Medicine. Easton, PA, 18042. The platinum based compounds are commonly used chemotherapeutic agents. Many agents in this class, such as Cisplatinum, are nephrotoxic. Oxaliplatin, a third generation based platinum compound, is a cytotoxic agent used in the treatment of recurrent colon and rectal cancers. We report a rare case of acute tubular necrosis (ATN) due to Oxaliplatin. An 82 year old female with a past history significant for recurrent rectal carcinoma and hypertension received four cycles of Folfox (Oxaliplatin/Leucovorin/5FU) at a dose of 85mg/m2. She experienced significant improvement in her cancer burden. One week after her fourth cycle of chemotherapy she presented to the hospital with increasing shortness of breath and lower extremity edema. She denied any nausea, vomiting, or diarrhea. Labs showed acute kidney injury (AKI) with a creatinine of 4.5mg/dl. Prior to beginning the chemotherapy, she had a creatinine of 0.8 mg/dl. During the hospitalization, her renal function worsened and with a creatinine of 7.5mg/dl hemodialysis was initiated. A 24 hour urine protein showed tubular range proteinuria of 141mg. Serologic workup including complements was negative, and there was no peripheral or urine eosinophilia. A renal ultrasound showed parapelvic cysts, mild cortical thinning, and no hydronephrosis. A triple- phase renal flow scan with technetium showed diminished perfusion of both kidneys with moderately reduced function of both kidneys in a symmetrical pattern consistent with ATN. Over the next two weeks, she improved and dialysis was discontinued. Her creatinine has decreased so far to a value of 1.3mg/dl. An extensive review of the literature only shows two case reports of oxaliplatin induced AKI. Based on the above , we believe that her AKI was due to the Oxaliplatin.. We wonder if there may be a circulating metabolite that may be nephrotoxic given that the cumulative dose of four cycles is significantly less than other described regimens, and that each individual dose was calculated based on ideal body weight. We feel that Oxaliplatin should be considered as a nephrotoxic agent along with the other platinum based compounds. INCIDENCE AND PREDICTORS OF ACUTE RENAL FAILURE IN PATIENTS HOSPITALIZED FOR CONGESTIVE HEART FAILURE Harini Chittineni, Sailaja Gulipelli, Eduard Bover, Joseph Roglieri, Steven Fishbane. Winthrop-University Hospital, Mineola, NY, USA Congestive heart failure (CHF) is a common cause for hospital admission. Patients often develop acute renal failure which may lengthen hospital stay and increase risk for adverse outcomes. The purpose of this study was to describe the incidence of acute renal failure (ARF) in hospitalized patients with CHF, and to determine predictors for its occurrence. Chart review was conducted of 508 consecutive admissions to a community hospital with principal discharge diagnosis of CHF from 2004. A variety of demographic, clinical and echocardiographic parameters were studied. Increase in serum creatinine (SCr) of ≥0.5 mg/dL occurred in 106/508 (20.8%) of patients, SCr increase of ≥1.0 mg/dL in 21 (4.1%) patients, ≥2.0 mg/dL in 7/508 (1.4%). ARF (SCr increase 0.5 mg/dL) developed on day 2-(10.3%), day 3- (19.8%), day 4- (18.8%), day 5- (24.5%), day 6- (25.4%). The risk of ARF (defined as increase SCr 1.0 mg/dL) was increased among patients with lower admission sodium (133.5±6.1 meq/L vs. 138.6±4.5 meq/L, p<0.0001), higher admission serum creatinine (1.7±0.9 mg/dL vs. 1.4±0.6 mg/dL, p<0.0001), and patients with echocardiographic diastolic dysfunction (52.3% vs. 18.0%, p=0.006). Other variables close to reaching statistical significance included IV diuretic use day 1, (95.2% vs. 81.7%, p=0.14) and diabetes mellitus (52.3% vs. 34.3%, p=0.10). Use of ACEI/ARB after admission did not increase the risk of ARF (52.3% vs. 53.5%). In conclusion, acute renal failure is a common complication in patients hospitalized for CHF. Its risk is increased among patients with diastolic dysfunction who are hyponatremic and have elevated serum creatinine at admission. ROLE OF BNP LEVEL IN THE ASSESSMENT OF VOLUME STATUS IN PATIENTS WITH ADVANCED LIVER DISEASE AND ACUTE RENAL FAILURE Frederick Fleszler¹, Rasib Raja¹, Carlos Ferran². ¹Nephrology, Albert Einstein Medical Center, Philadelphia, PA, USA; ²Penn State University, Malvern. PA, USA. Most patients with advanced liver disease have clinical evidence of volume overload but they may be intravascularly volume depleted. Assessment of the volume status is challenging in this clinical setting. Blood BNP levels are being used for determination of volume status increasingly. This study was performed to determine the correlation between BNP levels and urine parameters in the assessment of the volume status in patients with advanced liver disease and acute renal failure. This is a retrospective study conducted between December 2004 and September 2005. Patients with anuria, requiring emergent dialysis, creatinine < 1.4 mg/dl, recipients of liver and/or kidney transplant and without complete laboratory data were excluded. Thirty- two patients met the inclusionary criteria (age 18-70 yrs). Initial volume status was determined based on clinical findings: neck veins, edema, skin turgor and mucus membranes characteristics. Demographic and laboratory data were collected at the time of initial evaluation. Patient’s outcome was recorded: improvement of renal function, no change, requirement of dialytic therapy and death. Results were analyzed by Pearson Correlation and Chi-square using SPSS software. Patients were stratified as prerenal (n=9), hepatorenal (n=15) and acute tubular necrosis (n=8) Mean FeNa was 0.37, 0.42 and 2.08; Mean FeUrea was 19.68, 24.02 and 43.64; Mean BNP level was 155.67, 390.47 and 390.01 respectively. Based on the clinical assessment, the patients were divided into three groups: volume depleted (n=16), euvolemic (n=11) and volume overloaded (n=5). BNP levels did not correlate with the clinical assessment of the volume status (P = 0.09) nor with FeNa and FeUrea (P = 0.84 and 0.96 respectively) nor patients’ outcome (P =0.43). These data suggest that BNP has limited value for assessment of volume or outcome in patients with advanced liver disease and acute renal failure. Urinary indices with clinical response to hydration may help differentiate amongst different etiologies for the ARF. STILL CONSIDER POSTPARTUM URINARY RETENTION DESPITE NO CHANGE IN URINE OUTPUT Monica Grafals, Michael Dunn, Ahmed Mian, Naveen Gupta, Meenal Shah, Ziauddin Ahmed, Karthik Ranganna, Irene Toh. Drexel University College of Medicine, Philadelphia PA, USA Postpartum urinary retention is a common complication in the early puerperium. There is no standard definition, but it is usually not associated with spontaneous micturation within 6 hours of vaginal delivery, or post-foley removal after C-section. We report a case of postpartum urinary retention which reportedly had no change in voiding pattern or urine volume. Case Report: A 24 y/o Asian female (G2P2) with no past medical history and a normal pregnancy had an uneventful C-section. She received epidural anesthesia, and per protocol, the bladder catheter was removed 12 hours post surgery. She received IV ketorolac for pain. The next day she presented with abdominal discomfort and distention. There was no reported change in urinary volume or pattern. Serum creatinine rose from 1mg/dL to a peak of 5mg/dL. Urinalysis was unremarkable. CT of the abdomen revealed anasarca. Ultrasound was negative for hydronephrosis and doppler showed intact blood flow.
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