Salicylate Poisoning and Rebound Toxicity.

Salicylate exposure and toxicity are associated with a myriad of symptoms and signs, and a comprehensive knowledge of diagnosing and treating salicylate poisoning is needed. Here, we present a case of a 29-year-old female with a past medical history of schizoaffective disorder and bipolar disorder with multiple suicide attempts brought to our hospital, Nassau University Medical Center, East Meadow, by the Emergency Medical Service (EMS) due to an intentional overdose of 300 pills of acetylsalicylic acid. She had mixed acid-base disturbance with respiratory alkalosis and metabolic acidosis. She was started on bicarbonate infusion in the emergency department to maintain a blood pH of 7.5 and to maintain a urine pH of more than 7.5. As her salicylate levels were 98.2 at admission with altered mental status, she was started on slow, low-efficiency hemodialysis. A few hours later, she developed a rebound increase in salicylate levels to 129, associated with a change in mental status and the patient was more confused. She was started on regular hemodialysis with improvement in mental status and elimination of salicylate steadily. Given the extensive nature of toxic effects, a patient with severe salicylate toxicity can deteriorate rapidly and can be challenging to manage. As there is no specific antidote for aspirin, the goals of therapy depend primarily on limiting the absorption of salicylate, enhancing elimination, and providing supportive care. Monitoring the acid-base status and serum salicylate levels closely and monitoring for rebound increase in salicylate levels is of paramount importance. Aggressive hydration to maintain euvolemia, alkalinization, aggressive replenishment of potassium and magnesium, activated charcoal to decrease absorption, and hemodialysis remain the cornerstones of treatment.

Unusual Clinical Presentation of Nephrotic Syndrome With Significant Renal Vein Thrombosis in a Young Male: A Case Report and Literature Review.

Primary membranous glomerulopathy is the most common cause of idiopathic nephrotic syndrome, with increasing recognition as an autoimmune-mediated disease. We present the case of a 31-year-old Hispanic male with no prior medical or family history, presenting with one month of dyspnea on exertion, lower extremity, and periorbital edema with a recent diagnosis of pulmonary embolism. Upon further imaging, renal vein thrombosis was discovered with significant lab dysfunction concerning nephrotic syndrome. Further, a workup of kidney biopsy and serum antibody levels revealed the cause to be anti-phospholipase A2 receptor (PLA2R)-mediated.

When Overdose of Doxylamine Leads to Severe Rhabdomyolysis and Renal Failure That Requires Hemodialysis: A Case Report and Literature Review.

A 52-year-old male with acute onset right-sided weakness, numbness, and buttock pain after consuming 30 tablets of doxylamine antihistamine the night prior. Laboratory tests showed elevated creatinine kinase, blood urea nitrogen, creatinine, troponins, liver transaminases, and phosphate. The patient was admitted to the medical intensive care unit for severe rhabdomyolysis, acute liver failure, and acute kidney injury secondary to doxylamine intoxication. Studies describe symptoms of severe doxylamine intoxication, such as impaired consciousness (coma), grand mal seizures, and cardiopulmonary arrest. Circulating myoglobin causes oxidative injury to the kidney through the formation of F2-isoprostanes leading to renal vasoconstriction. One study explained drug-induced rhabdomyolysis via two mechanisms: direct drug injury to the striated muscle and local muscle compression in seizure, coma, and metabolic abnormality. Treatment involves aggressive hydration with monitoring of serum electrolytes and renal function. Aggressive volume expansion via intravenous fluids remains critical in preventing rhabdomyolysis-associated nephrotoxicity and myoglobin-induced acute renal failure. Alkalinization of urine may prevent renal vasoconstriction resulting in enhanced excretion of the toxic metabolites of doxylamine and myoglobin via renal tubules, thereby reducing peak serum concentration time and preventing direct renal tissue damage.

An Oncological Emergency: Severe Type B Lactic Acidosis From Warburg Effect in Diffuse Large B-cell Lymphoma.

Lactic acidosis is the most common anion gap metabolic acidosis in critically ill patients. Type B lactic acidosis is most commonly seen with hematological malignancies, especially lymphomas. It is considered an oncological emergency and is associated with high mortality and poor outcomes if not treated promptly. Here, we present the case of a 48-year-old male who developed Type B lactic acidosis secondary to newly diagnosed diffuse large B-cell lymphoma. This case highlights the importance of including Type B lactic acidosis in the differential diagnosis in a patient with unexplained lactic acidosis and hypoglycemia with otherwise vague symptoms and the need for a thorough search for quick diagnosis and early management.

Atypical hemolytic uremic syndrome: when pregnancy leads to lifelong dialysis: a case report and literature review.

Atypical hemolytic uremic syndrome (aHUS), a challenging disorder, commonly caused by inherited defects or regulatory processes of the complement alternative pathway. There are multiple causes, including pregnancy. Pregnancy provokes life-threatening episodes, preeclampsia, hemolysis elevated liver enzymes low platelets, microangiopathic hemolytic anemia (MAHA) and end-stage renal disease. Additionally, complement dysregulation and, with aHUS, affects fetal and maternal outcomes. Pregnancy-associated aHUS results in a poor prognosis with irreversible renal damage. Likewise, it is imperative to know that MAHA can provoke endothelial disruption, destruction of red cells and thrombocytopenia. We present a case of a young 18-year-old woman with MAHA and aHUS, requiring emergent cesarean section at 34 weeks of gestation and hemodialysis, secondary to complications from a recent pregnancy. Elevated blood pressure readings, rising creatinine levels, as well as her mother being on dialysis after pregnancy raised suspicion for thrombotic microangiopathy and aHUS. She was subsequently managed with plasma exchange, steroids, eculizumab and hemodialysis. Thus, plasma exchange should be initiated, with pending additional workup. Upon a definitive diagnosis of aHUS, eculizumab would be warranted to mitigate immune dysregulation. Understanding thrombotic microangiopathies diagnosis, and recognizing concomitant consequences, is vital. Having better insights into endothelial injuries can prevent unfortunate outcomes.

Mortality in Living Kidney Donors With ESRD: A Propensity Score Analysis Using the United States Renal Data System.

INTRODUCTION: In recent years, data have emerged on the outcomes of living kidney donors who develop end-stage renal disease (ESRD). We aimed to evaluate mortality rates in kidney donors who had initiated dialysis compared with a propensity-matched cohort of dialysis patients without previous kidney donation. METHODS: We used the United States Renal Data System (USRDS) and abstracted 274 previous living kidney donors between 1995 and 2009. There were 609,398 individuals on dialysis without kidney donation. We used propensity score matching to identify 258 donors and 258 nondonors. The time-dependent Cox proportional hazards model was used to compare survival between the 2 matched cohorts. RESULTS: In the propensity score-matched cohort, mortality was lower in donors compared with nondonors (19% vs. 49%; P < 0.0001). The time-dependent Cox proportional hazards model demonstrated that donors had significantly lower mortality compared with nondonors 0 to 5 years since start of dialysis (hazard ratio [HR]: 0.17; 95% confidence interval [CI] 0.11-0.27; P < 0.0001) and with nondonors 5 to 10 years on dialysis (HR: 0.34; 95% CI: 0.19-0.63; P < 0.001). We were unable to estimate the difference between the 2 groups after 10 years on dialysis with any precision (HR: 0.51; 95% CI: 0.18-1.42; P = 0.20) due to the small sample size. CONCLUSION: We observed a lower mortality rate in living kidney donors with ESRD compared with matched nondonors. This data should guide clinicians in the informed consent process with prospective donors.