Setting Of Acute Renal Failure Research Articles

THU278 Hidden In The Immune System: Exogenous Insulin Antibody Syndrome In A Patient With Latent Autoimmune Diabetes In Adults

Abstract Disclosure: H.L. King: None. R. Nagappan: None. A. Sliwinska: None. Hidden in the Immune System: Exogenous Insulin Antibody Syndrome in a Patient with Latent Autoimmune Diabetes in Adults Background: Exogenous insulin antibody syndrome (EIAS) is a rare syndrome associated with insulin antibodies induced by exogenous insulin, found predominantly in patients with type 2 diabetes using various insulin formulations. Here, we present a case of young man previously diagnosed with type 2 diabetes, who was found to have severe refractory diabetic ketoacidosis (DKA) due to EIAS. Clinical Case: A 46-year-old man with a history of type 2 diabetes presented to an outside hospital for one week of fever and malaise. Laboratory studies were notable for serum glucose of 600 mg/dL (70-90mg/dL), HCO3 3 mmol/L (22-28mmol/L), and creatinine of 3.9 mg/dL (0.7-1.3mg/dL). He was diagnosed with DKA, shock and renal failure. During hospital stay, he remained on an insulin drip due to multiple unsuccessful attempts of transitioning to subcutaneous insulin, requiring over 1000 Units of insulin daily. This prompted insulin antibody testing that resulted elevated at >50U/mL (0-0.4U/mL), concerning for EIAS. Treatment was initiated with 5 days of IVIG and mycophenolate mofetil. During this treatment, his baseline insulin infusion rate of 30 Units/hr declined to 18 Units/hr, however at day 3, insulin requirements again increased. For better evaluation, quantitative insulin antibody values were requested and resulted as 362.5U/mL, followed by 350.9U/mL post IVIG treatment. After no significant improvement, patient was transferred to our hospital for further management of EIAS. Plasmapheresis was initiated followed by rituximab with plans for long term maintenance therapy. Dexamethasone was trialed but shortly after discontinued due concern of increased insulin resistance and hyperglycemia. Metformin was also started but discontinued due to concern of worsening acidosis in the setting of acute renal failure requiring CRRT. Ultimately, the patient was transitioned to subcutaneous U500 BID 75-150 Units based on scale. At discharge, metformin and pioglitazone were started. Due to the history of early onset insulin-dependent diabetes at age 30, he was tested for GAD-65 which resulted as positive at 0.28 nmol/L (<=0.02 nmol/L) and C peptide of 0.9ng/mL (0.8 - 3.9 ng/mL) consistent with LADA. Conclusion: EIAS is a rare and very challenging entity, increasing risks of severe ketoacidosis, hypoglycemic episodes and numerous other complications. Although mostly reported in type 2 diabetes, EIAS can occur in patients with LADA suggesting that autoimmunity may play a role. There is no FDA approved treatment, however attempts focus on eliminating antibodies by plasmapheresis, IVIG and immunotherapeutic agents. Presentation: Thursday, June 15, 2023

HOW LOW CAN YOU GO: RECOVERY AFTER A SERUM PH OF 6.62 DUE TO ETHYLENE GLYCOL POISONING

HOW LOW CAN YOU GO: RECOVERY AFTER A SERUM PH OF 6.62 DUE TO ETHYLENE GLYCOL POISONING

Abstract #1168985: Euglycemic Ketoacidosis and Lactic Acidosis Associated with Metformin Toxicity

Metformin-associated lactic acidosis (MALA) in the setting of acute renal failure is well documented, however, metformin-associated lactic acidosis and euglycemic ketoacidosis (MALKA) is less studied. With mortality rate reaching 50%, a high index of suspicion is required in patients who are taking metformin and presenting with acute renal failure and euglycemia.

Safety and Tolerability of Fedratinib (FEDR), an Oral Inhibitor of Janus Kinase 2 (JAK2), in Patients with Intermediate- or High-Risk Myelofibrosis (MF) Previously Treated with Ruxolitinib (RUX): Results from the Phase 3b FREEDOM Trial

Safety and Tolerability of Fedratinib (FEDR), an Oral Inhibitor of Janus Kinase 2 (JAK2), in Patients with Intermediate- or High-Risk Myelofibrosis (MF) Previously Treated with Ruxolitinib (RUX): Results from the Phase 3b FREEDOM Trial

Acute liver failure and seizure: a case report of an unusual presentation of acute painless aortic dissection.

BackgroundPainless aortic dissection presenting with seizure and acute liver failure is uncommon. We described a case of early recognition leading to successful treatment of painless aortic dissection with atypical presentation.Case summaryA young lady presented with generalized tonic-clonic seizures coupled with hepatitic pattern of deranged liver function test. Examination revealed blood pressure of 99/75 mmHg and hepatic flap. Electrocardiography showed sinus tachycardia. Urgent bedside echocardiography showed preserved cardiac function without significant valvular pathology, but noted a moderate pericardial effusion. Abdominal Ultrasound excluded liver cirrhosis or biliary obstructions. Viral hepatitis serologies and anti-liver panel were negative. She was progressively hypotensive with concurrent acute liver failure and oliguric acute kidney injury. Despite no chest pain, her rising serum troponin and widened mediastinum prompted an urgent computed-tomography aortogram, which showed a 4.3 cm dilatation of ascending thoracic aorta with acute haemopericardium and cardiac tamponade. She was diagnosed with malperfusion syndrome from Stanford type A aortic dissection. She underwent emergent ascending aorta and aortic arch repair and dialysis. She experienced complete recovery in her kidney, liver, and neurological function post-operatively.DiscussionPainless aortic dissection masquerade as acute liver failure is uncommon. We describe a successful early recognition of malperfusion syndrome from painless aortic dissection, thus providing window for timely, life-saving intervention. Clinical challenges in this case include: (i) atypical presentation of aortic dissection, (ii) worsening acute liver failure which could lead to unnecessary liver transplantation, and (iii) risk of contrast-induced nephropathy in the setting of acute renal failure.

Monoclonal Gammopathy with Secondary Atypical Hemolytic-Uremic Syndrome

Monoclonal gammopathy is a clonal plasma cell disorder associated with an increased risk of progression to lymphoproliferative malignancy. In children, monoclonal and oligoclonal gammopathies are rare, and their clinical relevance unrecognized. Atypical hemolytic uremic syndrome (aHUS) is a rare endotheliopathy associated with dysregulated activation of complement, microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. We present a case of aHUS that we hypothesize was triggered by monoclonal gammopathy in a child several years after cardiac transplantation. An 11 year old African-American girl with sickle trait was transferred to our cardiac center with a two week history of epigastic pain, emesis, microcytic anemia, hypergammaglobulinemia, and development of renal failure requiring dialysis. She had undergone cardiac transplantation at 7 months of age for dilated cardiomyopathy of unknown etiology and had recovered from acute cardiac rejection requiring ECMO at age 5 years. She had previously experienced at least two episodes of acute kidney injury requiring dialysis with full recovery of function reported. Renal biopsy revealed a severe collapsing glomerulopathy and a thrombotic microangiopathy. Upon transfer to our institution, her labs were notable for microcytic anemia, normal platelet count, haptoglobin, and LDH. A week later, she developed aHUS diagnosed by hemoglobin 9.5 gm/dL, haptoglobin < 30 mg/dL, LDH 314 U/L, platelets 100,000, and a predominance of schistocytes on peripheral blood smear in the setting of acute renal failure. Serum protein electrophoresis (SPEP) revealed a monoclonal spike (1g/dL), identified as IgG kappa by immunoabsorption. A second, smaller monoclonal spike was identified as IgA lambda. aHUS evaluation revealed low C3, normal C4, and 50% CD46 expression by flow cytometry. Bone marrow biopsy with flow cytometry excluded lymphoproliferative disorders. EBV did not amplify with quantitative PCR of peripheral blood, and computed tomography imaging of the body did not detect abnormal mass or lymph nodes. A trial of plasmapheresis did not improve biochemical and hematologic features of aHUS. A trial of eculizumab resulted led to normalization of platelet count and C3, increased haptoglobin, reduced need for red cell transfusion, and less frequent dialysis. Monoclonal gammopathy of unknown significance (MGUS) is rare in children, but may be more common in transplant recipients, especially after cardiac transplants in infants when thymectomy is performed. MGUS associated with secondary aHUS has been rarely reported in adults. The mechanism for aHUS was demonstrated in one case to result from affinity of the paraprotein to a binding site on complement factor H, with subsequent loss of factor H cofactor activity to inhibit alternative complement activation. We hypothesize that immune dysregulation from fluctuating levels of paraproteins during inflammation in our patient with monoclonal gammopathy resulted in recurrent, intermittent episodes of aHUS. We speculate that this was responsible for the patient's collapsing glomerulopathy and dialysis-dependent chronic renal failure. This case highlights the importance of considering monoclonal gammopathy in pediatric patients who develop recurrent kidney failure or atypical hemolytic uremic syndrome in the setting of immune dysregulation. The merit of treating the monoclonal gammopathy with Bortezumib and Rituximab is currently under consideration. Disclosures No relevant conflicts of interest to declare.

COMMON LAB ABNORMALITIES FROM AN UNCOMMON SOURCE: A CASE REPORT

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Diffuse large B cell lymphoma (DLBCL) is an aggressive form of non-Hodgkin lymphoma (NHL) of B cells. Although its genesis is typically in the lymph nodes, it can form in extra-nodal sites such as the gastrointestinal tract and central nervous system. This disease usually presents with lymphadenopathy, fever, weight loss or fatigue. On occasion, this condition can also present with refractory hypoglycemia and lactic acidosis. CASE PRESENTATION: This is a case of a 66 year old female with a history of diabetes and DLBCL successfully treated with rituximab who presented with lethargy. Initial labs were remarkable for severe hypoglycemia and lactic acidosis of unknown origin. The patient was subsequently intubated, started on broad spectrum antibiotics and admitted to the intensive care unit. Her hypoglycemia was suspected to be secondary to glimepiride toxicity in the setting of acute renal failure and she was started on octreotide. However, her hypoglycemia was refractory to treatment. Her lactic acid continued to rise despite adequate fluid resuscitation and vasopressor support. Exploratory laparotomy was performed out of concern for mesenteric ischemia and revealed a necrotic appendix that was subsequently removed. Surgical pathology was consistent with recurrent DLBCL. Salvage chemotherapy was attempted with improvement in hypoglycemia and lactic acidosis; however, the patient ultimately succumbed to her illness several days later. DISCUSSION: DLBCL typically presents with nodal symptoms, fever, or night sweats. However, there have been a few documented cases of patients initially presenting with refractory hypoglycemia and worsening lactic acidosis despite adequate fluid resuscitation and vasopressor support. These findings presenting as a single entity has been associated with the Warburg effect, meaning that the high rate of replication and glycolysis in cancer cells ultimately leads to increased lactic acid formation and glucose consumption. In the setting of NHL, this is a rare complication and is associated with rapid disease progression and poor outcomes. CONCLUSIONS: This case is an example of an atypical etiology of common lab abnormalities. The patient had both hypoglycemia and an elevated lactate that were unresponsive to traditional therapies. Although a component of the patient's refractory hypoglycemia could have been due to glimepiride, its improvement with chemotherapy is consistent with it being related to DLBCL. In patients with refractory hypoglycemia and rising lactic acidosis with a history of malignancy, relapse should be considered as part of the differential diagnosis. Reference #1: Tanios G, Aranguren IM, Goldstein JS, Patel CB. Diffuse large B-cell lymphoma: A metabolic disorder? The American journal of case reports. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859735/. Published December 2, 2013. Accessed March 13, 2019. Reference #2: Vander Heiden MG, Cantley LC, Thompson CB. Understanding the Warburg effect: the metabolic requirements of cell proliferation. Science (New York, N.Y.). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849637/. Published May 22, 2009. Accessed March 13, 2019. DISCLOSURES: No relevant relationships by Soorya Aggarwal, source=Web Response No relevant relationships by Robert Decker, source=Web Response No relevant relationships by Breanna Goldner, source=Web Response No relevant relationships by Alaynna Kears, source=Web Response

Acute renal failure in the cardiac intensive care unit – A practical approach to management

The association between cardiovascular disease and acute renal failure (ARF) and acute-on-chronic renal failure is less well defined. In the cardiac intensive care unit (CICU), the presence of ARF imparts a significant mortality. The predominant aetiology of ARF in the CICU relates to hypotension, although other causes are certainly involved too, and both contrast nephropathy and cholesterol embolisation may be associated with percutaneous coronary intervention. Despite the availability of renal replacement therapies, preventative measures remain the most important element of management. Specific therapy includes management of the patient’s volume status, vasoactive medication and renal replacement therapy in the way of dialysis. In the setting of acute renal failure, both patient and renal outcome is improved with the early involvement of a nephrological service.

Invited Commentary on Treatment of Nocardia wallacei in an HIV Patient With Renal Failure

This is a case report of an HIV positive patient who was successfully treated with trimethoprim-sulfamethoxazole (TMP-SMX) for pulmonary nocardiosis in the setting of acute renal failure. TMP-SMX has been considered a mainstay of nocardiosis treatment for many years, although its use has traditionally been limited in the context of renal impairment. Alternative regimens have been shown to be effective in many cases of nocardiosis, although in our patient who developed acute kidney failure requiring dialysis his clinical status did not improve with other therapies. TMP-SMX ultimately was shown to be the most effective treatment and despite its risk of renal toxicity, the patient recovered renal function. This case also highlights the importance of early and aggressive treatment of nocardiosis to prevent invasive disease in immunocompromised individuals.

Dose-related effects of metformin on acid-base balance and renal function in patients with diabetes who develop acute renal failure: a cross-sectional study.

The role of metformin in the development of lactic acidosis (LA) in the setting of acute renal failure (ARF) is debated. Moreover, recent experiments suggested that metformin can also be nephrotoxic, but little clinical data exist about this topic. We sought to investigate these possible associations in a large cohort of patients with diabetes who developed ARF. We analyzed data from patients with diabetes admitted to our emergency department between 2007 and 2011 with ARF and a previously normal renal function (n=126). We compared acid-base balance and renal function of patients taking metformin (n=74) with patients not taking it (n=52). Patients taking metformin had decreased pH (7.31±0.16 vs 7.39±0.11, p=0.008) and higher lactates (4.54±4.30 vs 1.71±1.14mmol/L, p<0.001). Both acidosis (pH<7.35) and LA (lactates >5mmol/L and pH<7.35) were more frequently observed in this group (p=0.0491 and p<0.001, respectively). Multivariate analysis ruled out the role of some possible confounders, especially decreased renal function. The influence of metformin on pH and lactates grew significantly with higher doses of the drug (p=0.259 and p=0.092 for <1g/day, p=0.289 and p<0.001 for 1-2g/day, p=0.009 and p<0.001 for 2-3g/day, for pH and lactates, respectively). Metformin influenced creatinine levels in a dose-related manner as well (p=0.925 for <1g/day, p=0.033 for 1-2g/day, p<0.001 for 2-3g/day). In patients with diabetes who were admitted to our emergency department with ARF, the use of metformin was associated in a dose-related fashion with both LA and worse renal function.

Management of pulmonary vasodilator therapy in patients with pulmonary arterial hypertension during critical illness.

Pulmonary arterial hypertension (PAH) is commonly treated with pulmonary arteriolar vasodilator therapy. When a patient on PAH medication is admitted to intensive care, determining how to manage their medication during the critical illness is often complicated. There may be considerations related to the inability to take medication by mouth, related to acute renal failure or acute liver injury, related to altered mental status or delirium, or related to hypotension and bacteremia. Decisions of how to manage these medications can have a major impact on the patient’s clinical course. Presently, provider experience is the major tool in navigating the decisions regarding these medications. In this review, we offer our recommendations of how to manage PAH patients with critical illness who are on PAH medications. These recommendations include how to deliver medications via feeding tubes, how to dose medications in the setting of acute renal failure or acute liver failure, and how to manage medications during hypotension or when a tunneled catheter needs to be removed.

Pseudo empty delta sign due to poor clearance of intravenous contrast in the setting of acute renal failure

Pseudo empty delta sign due to poor clearance of intravenous contrast in the setting of acute renal failure

Pediatric Cefepime Neurotoxicity

Cefepime toxicity is characterized by altered mental status, confusion, and decreased responsiveness. We describe a 14-year-old girl who developed acute encephalopathy associated with supratherapeutic cefepime concentrations in the setting of acute renal failure. The authors were unable to identify any previous reports of this occurrence in a child.

Peri-operative renal protection: The strategies revisited.

Postoperative acute renal failure (ARF) is a serious complication which can result in a prolonged hospital stay and a high mortality and morbidity. Underlying renal disease, cardiac diseases, nephrotoxin exposure and renal hypoperfusion are the possible predisposing risk factors which can create a high probability for the development of ARF. The incidence of ARF is highest after major vascular, cardiac and high-risk thoraco-abdominal surgery. Among the various renal protection strategies, adequate peri-operative volume expansion and avoidance of hypovolemia is the most accepted and practiced strategy. Numerous bio-markers of renal injury are used to estimate the presence and extent of renal insult and various new are currently under trial. Traditional pharmacological interventions like dopamine, diuretics and calcium antagonists are not currently the first line of reno-protective agents. The new non-pharmacological and pharmacological methods may improve outcome in renal transplantation, contrast-induced nephropathy and in various other settings of ARF. The current review is an attempt to refresh the knowledge and put forth the various renal protection strategies during the peri-operative period.

Acute Transplant Glomerulopathy is Associated With Antibody-Mediated Rejection and Poor Graft Outcome

Transplant glomerulopathy (TG) is traditionally considered to be a chronic entity. However, in our practice we observed patients who presented with features of TG as early as 14 days posttransplantation. We investigated the clinicopathological features of these cases. During a 4-year period, all patients with acute rejection were identified. Charts were reviewed to identify patients with antibody-mediated rejection and biopsy features of TG within 6 months posttransplantation. Three patients met the above- mentioned criteria. All of them had diffuse margination of inflammatory cells in peritubular capillaries in the setting of acute renal failure or delayed graft function. Monocyte (CD68-positive) margination in peritubular capillaries was a common feature. All 3 patients had donor-specific antibodies and features suggestive of antibody-mediated rejection. C4d stain in peritubular capillaries was focal and mild or absent in serial biopsies. Occlusive endothelial swelling of glomerular capillary loops (endotheliosis) preceded TG. None of the patients had evidence for other causes of similar glomerular changes in a transplant, such as calcineurin inhibitor toxicity, ischemia, hepatitis C, or immune complex glomerulonephritis. They did not have other biopsy features of chronicity when TG appeared and as it progressed. TG can occur as an acute phenomenon. We propose that endotheliosis is a more accurate and specific precursor of TG than mere glomerulitis. These cases of acute TG may represent a form of antibody-mediated rejection associated with proteinuria and poor response to treatment.

Nephrogenic systemic fibrosis following acute kidney injury and exposure to gadolinium

Nephrogenic systemic fibrosis (NSF) is a scleroderma-like systemic fibrosing condition of unknown etiology described in patients with renal insufficiency. Gadolinium exposure has been strongly associated with the development of NSF though the mechanism of such injury is not known. There are only few reported cases of NSF in the setting of acute renal failure and fewer reported cases where skin lesions developed after kidney function had returned to normal. We report a case of NSF in a young Hispanic woman with lupus nephritis but normal creatinine, who received gadolinium during a brief episode of prerenal acute kidney injury not requiring dialysis, secondary to sepsis.

How to perform a haemodialysis using the arterial and venous lines of an extracorporeal life support

Continuous renal replacement therapy is particularly suited in the setting of acute renal failure, occurring after cardiac surgery, in patients requiring extracorporeal life support (ECLS) or membrane oxygenation. In such patients, temporary catheters are not necessary since the circuit of haemodialysis or haemofiltration may be connected on the ECLS cannulae. We report how to modify a classical ECLS circuit to connect directly the haemodialysis (Prismaflex device, Gambro-Hospal, Lyon, France) to the ECLS. We also detail parameters used to initiate the haemodialysis. Actually, we modify all our ECLS circuits as described here, at implantation time, allowing rapid haemodialysis initiations. Since 2004, 21 patients have been treated, as described here, without supplemental mortality or related complication.

Percutaneous revascularization of occluded renal arteries in the setting of acute renal failure

We report the case of a 60-year-old patient with acute renal failure and occluded bilateral renal arteries presenting with acute pulmonary edema and non-ST segment elevation myocardial infarction. The patient required renal replacement therapy with hemodialysis and was subsequently successfully treated with bilateral renal artery stent placement. Marked improvement in renal function was noted within 1 week with freedom from the need for renal replacement therapy at 4 months of follow-up.

Delayed Kounis syndrome and acute renal failure after wasp sting

A fifty-seven year old gentleman developed hemolysis induced oliguric acute renal failure following multiple wasp stings. Patient was hemodynamically stable on dialytic support. Twelve days later, although the patient was recovering from renal failure, he developed sudden onset of tachyarrythmias and echocardiography demonstrated a Takotsubo type of cardiomyopathy. He was managed with amiodarone and hemodialysis. After two more episodes of deterioration, the patient made full recovery from both the renal and cardiac toxicity. A case of delayed Kounis syndrome associated with Takotsubo cardiomyopathy in the setting of acute renal failure is described. The possible mechanism of such a presentation is discussed.

Predictors of Mortality in a Cohort of Intensive Care Unit Patients With Acute Renal Failure Receiving Continuous Renal Replacement Therapy

Despite the frequent use of continuous renal replacement therapy (CRRT) in the management of acute renal failure (ARF) in the critically ill, predictors of mortality remain unclear. A registry of all patients initiated on CRRT at a single institution was assembled over an 18-month period, and a subsequent cross-sectional analysis of selected variables was conducted for associations with mortality. Predictors evaluated were age, gender, diagnosis of sepsis, Apache II score, days between ARF diagnosis and initiation of CRRT, creatinine at initiation of CRRT, change in creatinine from baseline and admission to initiation of CRRT, setting of ARF, and prescribed CRRT dose. The principal outcome was mortality at 30 days. Eighty-one individuals met inclusion criteria. Overall mortality for the study was 50.2%. The mean elevation in creatinine from admission to initiation of CRRT was 1.6 mg/dL (141.4 micromol/L) in those who lived and 2.6 mg/dL (229.8 micromol/L) in those who died (P = 0.023). Patients admitted with normal renal function who developed ARF while in the hospital had mortality of 56.3%. When available, patients with abnormal renal function at presentation were further classified by either abnormal or normal preadmission creatinine. These patients had mortality of 31.3% and 83.3%, respectively. These differences in mortality were statistically significant. Increased mortality was significantly associated with the magnitude of change in serum creatinine between admission and initiation of CRRT. Also, patient ARF classification was significantly associated with mortality.