Partial Nephrogenic Diabetes Insipidus Secondary to Lithium Use

Introduction: Nephrogenic diabetes insipidus (NDI) is caused by reduced renal response to vasopressin. NDI affects up to 40% of patients on lithium. We present a case of partial NDI secondary to lithium use. Case Description: A 66 year old male with bipolar disorder on lithium presented with shortness of breath, chest tightness and cough. On exam he was cachectic, lethargic, tremulous with decreased skin turgor and dry mucous membranes found to have COVID-19 with initial unremarkable blood work. Received treatment for COVID and subsequently developed worsening encephalopathy, follow up blood work revealed elevated serum sodium of 168 mg/dl, with urine osmolality of 382 and lithium level was elevated at 1.6 mEq/L. He received adequate IV fluid hydration with hypotonic fluids and free water. Serum sodium remained elevated with polyuria. Follow up labs showed urine osmolality decrease to 94 mosml/L therefore nephrogenic diabetes insipidus was suspected. A desmopressin stimulation test was performed and hourly urine osmolality was obtained [Table 1] confirming the diagnosis of nephrogenic diabetes insipidus with a partial response to desmopressin compatible with lithium-induced partial diabetes insipidus. Treatment was started initially with chlorthalidone with inappropriate response, then dose increased to 100mg daily with further addition of amiloride 10mg twice daily with subsequent response and decrease of sodium level from 167 to 147 mEq/L. Discussion(s): Lithium-induced NDI is explained by downregulation of aquaporin 2 channel expression in the principal cells due to accumulation of toxic concentrations of lithium and reduction of the kidneys' ability to preserve water in response to vasopressin. NDI usually presents with polyuria, polydipsia, severe dehydration, and electrolyte imbalance. A less than 50% increase in urine osmolality following desmopressin administration proves NDI. Treatment options include high doses of desmopressin, low sodium diet, thiazide diuretics, amiloride, and NSAIDs. (Table Presented).

A case of severe hyponatremia in a patient with COVID-19

Introduction: Hyponatremia is a common electrolyte disturbance seen in association with conditions such as malignancy and infections. In the recent literature, hyponatremia has been linked to SARS-CoV2 infection. To date, the most likely reported etiology of hyponatremia in setting of COVID-19 has been SIADH. We describe a severe case of hyponatremia, not due to SIADH, seen in a patient with COVID-19 Case Description: 49-year-old male with history of hypertension, hyperlipidemia, positive novel coronavirus nasopharyngeal swab done as outpatient, presented to the emergency department with fever, cough and dyspnea for a week. On admission, he was afebrile with respiratory rate of 18 and oxygen saturation of 84% on ambient air. His BP was not low, and heart rate ranged from 95-105 beats per minute. Pulmonary examination revealed rales bilaterally. Initial laboratory test showed serum sodium of 104 mEq/L and serum creatinine 0.58 mg/dL. Additionally, C-reactive protein was elevated to 7.19, serum ferritin elevated at 1798 and D-dimer was 158. CXR showed bilateral infiltrates. Serum osmolality was low at 217, and urine studies showed elevated urine osmolality (328) and low urine sodium (< 35), suggestive for diagnosis of hypotonic hyponatremia from volume depletion. He received treatment with 3% hypertonic saline with a subsequentdecrease in urine osmolality to 83. Serum sodium rapidly corrected to 118 requiring hypotonic fluids to manage overcorrection. Subsequently, serum sodium improved to a level of 133 mEq/L in the next 5 days after admission Discussion: As the COVID-19 pandemic continues to evolve, cases of related hyponatremia in this setting are being reported, mostly SIADH being the underlying etiology. Various mechanisms for SIADH development, including cytokine storm, and hypoxic pulmonary vasoconstriction have been postulated, however, the common aspect of volume depleted state in setting of viral infection, leading to appropriate ADH release should not be forgotten.

First us case series: Continuous renal replacement therapy with adsorbent oxiris filter in the setting of COVID-19 infection

Introduction: Many COVID-19 hospitalized patients sustain acute kidney injury (AKI) requiring CRRT. Multisystem hyperinflammatory response plays a large role in their infection leading to enhanced morbidity and filter clotting. Oxiris filters have been used for years in Europe in septic patients due to their properties of reducing cytokines and inflammatory mediators but have not been available in the United States until late April 2020. Use of these filters in COVID-19 patients has been very limited, and has not yet been reported. We report the first U.S. experience in 3 COVID-19 patients requiring mechanical ventilation for their respiratory failure and continuous venous to venous hemodiafiltration (CVVHDF) using oXiris dialyzers for their (AKI). Case Description: Case 1: A 73 year old male with laboratory tests revealing: creatinine 1.79mg/dl, C-Reactive Protein 1.01mg/dl, D-dimer 597, ferritin 13,000 ng/ ml and Interleukin-6 (IL-6) 96 pg/mL. He was started on CVVHDF with M150 filter and then switched to oXiris filter. He remained on oXiris CVVHDF for 9 days with no reported clotting events, a decline in ferritin by 90% to 1437ng/mL and a decline in IL-6 levels to 73 pg/mL. Case 2: A 55 year old male on CVVHDF with the M150 filter had a serum ferritin level progressively increasing to 2377 ng/ml and multiple clotting events. The dialyzer was switched to oXiris. He had no clotting events while on CVVHDF for six days and his serum ferritin level decreased to 1759 ng/ml. Case 3: A 40 year old male on extracorporeal membrane oxygenation (ECMO). He was initiated on CVVHDF to the ECMO circuit using a M150 filter for 7 days and was switched to oXiris filter with no reported clotting events thereafter. Discussion: The COVID-19 cytokine storm leads to activation of pro-inflammatory mediators leading to severe morbidity including coagulopathic events. Optimal treatment is still unknown. ECMO and CVVHDF with oXiris dialyzer in critical COVID-19 infection may play a role in decreasing inflammatory markers, which confers overall clinical improvement. Once switched to oXiris, our patients showed improvement in inflammatory markers and had no clotting of their dialyzers. In these patients, convective clearances (CVVHDF) may be more beneficial than diffusive therapies (CVVHD).

Thrombotic microangiopathy (TMA) in a patient with COVID-19

Introduction: We describe a patient with COVID-19 and clinically significant kidney biopsy proven TMA Case Description: 69-year-old Caucasian female with medical history of asthma came to the ED with productive cough, fever and dyspnea for 2 weeks. She was afebrile, tachypneic and hypoxic. Initial laboratories showed a normal WBC, hemoglobin level and platelet count. Inflammatory markers were elevated. SARS-CoV-2 infection was confirmed by PCR assay. CXR showed bilateral diffuse patchy opacities. Treated with hydroxychloroquine, enoxaparin and oxygen was started. Patient received anakinra and tocilizumab. On day 12, the patient developed thrombocytopenia, anemia and worsening kidney function concerning for microangiopathic hemolytic anemia. Due to worsening hypoxemia, patient received convalescent plasma. On day 17, she was intubated due to worsening respiratory failure. Findings suggestive of hemolysis were present. Urinalysis showed hematuria and proteinuria. Patient's kidney function worsened requiring initiation of CRRT. On day 20, the patient underwent a kidney biopsy that revealed severe acute TMA with cortical necrosis. Beta 2 glycoprotein-1 IgM levels were elevated, antiphospholipid antibodies were absent. A disintegrin and ADAMTS13 level were not low. C3,C4 were in normal range. Heparin induced antibody testing was negative. Coagulation parameters were normal. Kidney doppler was unremarkable. No other systemic findings of macro thrombi were found. Low factor H complement antigen, elevated plasma CBb complement and plasma SC5b-9 complement levels suggesting an activation of the alternative complement pathway were found. Genetic testing was not done. Plasma exchange was not performed, but received a single dose of eculizumab on day 21. Unfortunately, she died on day 23. Discussion: Coagulopathy associated with SARS-CoV-2 has been widely reported. Profound hypoxia, inflammation, disseminated intravascular coagulation(DIC) have all been implicated as potential causes, but were not present in our patient. To the best of our knowledge, we report the first case of TMA associated with SARS-CoV-2 with presence of diffuse cortical necrosis and widespread microthrombi in kidney biopsy. It is not clear if the virus played a direct pathogenic role or unmasked a latent complement defect leading to widespread endothelial damage and micro thrombi.

Slow low-efficiency dialysis (SLED) implementation during the COVID-19 pandemic surge

Background: The high rate of ARF in COVID-19 hospitalized patients increased the demand for critical care renal replacement therapy 2-3 fold at Northwell Health (NW). At the 2 largest hospitals, Long Island Jewish (LIJ) and North Shore University Hospital (NSUH), bedside HD was provided by HD RNs and continuous renal replacement therapy (CRRT) by critical care (CC) RNs. RN workload in these hypercatabolic patients soared as HD treatments more than doubled and CRRT increased from 9 to 30,. Shortages of CRRT fluid and filter sets ensued. SLED, a technique utilizing standard HD dialysate and filters, combined with a collaboratiive approach between CC and HD RNs was considered. Methods: In late March, a cohort CC bedside HD program, was initiated. Based on this success, a leadership panel of CC/HD RN and Renal/CC MDs created a SLED project plan. Details were reviewed with stakeholders on Friday prior to the Tuesday “Go-Live.” 3 patients previously treated with HD or CRRT via a Shiley catheter were selected as a pilot for three 6-8 hour sessions, Fresenius 2008T, Revaclear 300 filters with dialysate flow rate 300 cc/min and blood flow rate 200-300 cc/min were ordered. HD RN initiated treatments and available throughout, while clinical stability was monitored by CC RN. Results: NSUH pilot involved 5 patients over 3 sessions. Suboptimal cohorting required remote tablet monitoring and frequent presence of several HD RNs. One patient was terminated in one session due to persistent hypotension. Clearances and UF goals were achieved throughout. A week later the LIJ pilot used the design and advantage of NSUH experience with a 3 bed “SLED Room” model. The same 3 patients participated in all 3 sessions supervised by a single HD RN with no discontinuation. CC RN satisfaction with SLED was ranked “high” at both sites and by LIJ HD RNs but “Spread SLED” rated only “fair” by NSUH HD RNs. Pilots were extended 10 days. During this period SLED was initiated at 2 other NH sites. Future SLED programs will be focused on NH hospitals lacking CRRT. Conclusions: SLED is an efficient alternative to CC HD and CRRT. The challenges of effective cohorting in a pandemic surge relegate its role to a piece of a comprehensive renal critical care program. It imay be particularly valuable for hospitals lacking CRRT options.