Precipitous AKI due to acute renal artery thrombosis in a patient with protein s deficiency

Introduction: Renal arterial thrombosis and infarction is an under-recognized condition due to its rarity and ability to mimic other disease processes. It can lead to secondary hypertension, acute kidney injury, and chronic kidney disease. Clinical manifestations include nausea, vomiting, flank pain, and sudden elevations in blood pressure. Here, we present a case of a patient with previous normal kidney function presenting with a severe AKI due to an acute renal arterial thrombus. Case Description: A 58-year-old woman with previously normal kidney function (baseline Cr of 0.8 mg/dL) presented with complaints of nausea and vomiting and was found to have a stage 3 AKI with a creatinine of 4.65 mg/dL. Her creatinine level continued to rise, peaking at 8.5 mg/dL, despite volume expansion. Her urinalysis showed moderate blood and moderate protein. Her FeNa was calculated to be 6.5% and the P/creatinine was found to be 4.56 grams. Renal ultrasound revealed right renal atrophy and a normal appearing left kidney. She remained non-oliguric with good urine output and initially did not meet requirements for renal replacement therapy. Due to the unknown etiology of her AKI, a left kidney biopsy was performed which revealed fulminant acute cortical necrosis. Subsequently, an MRA revealed complete occlusion of the left renal artery. No angioplasty or stent placement was performed, and she eventually required renal replacement therapy. Hypercoagulable testing revealed protein S deficiency. Other serologic work up was negative. She was tested multiple times for COVID19 infection during her hospital stay and each test was negative. Discussion: The majority of renal thromboembolisms originate as emboli from the heart. Much less commonly, thrombi may form in the renal arteries themselves, especially in those with a hypercoagulable state such as this patient. In light of the recent global COVID19 pandemic, renal artery thromboembolism has gained increased recognition and prevalence. As such, our patient tested negative multiple times for COVID19 as a potential explanation for her hypercoagulable state. Acute renal artery thrombosis should be considered as an explanation for AKI of unknown etiology, especially in those who have underlying risk factors. In the appropriate context, imaging studies should be obtained promptly to prevent permanent kidney injury.

Cause or not: IGA-dominant infectious-related glomerulonephritis in a patient infected with COVID-19

Introduction: IgA dominant infectious related glomerulonephritis (IGAD-IRGN) is an uncommon variant of IRGN. It has been mostly associated with S.aureus infections. In the COVID Era, thre has been one case of IGAD-IRGN related to COVID. This is a case of IGA-IRGN in a patient infected with COVID-19. Case Description: 51 y/o male with no previous medical history who presented with a 3 day history of generalized swelling. Patient had no known medical problems and was not taking any medications. He reported drinking 3 beers daily. Denied any recent illness or sick contacts. At ED, the patient was found with anasarca and uncontrolled blood pressure. Initial blood tests showed normal renal function with hypoalbuminemia (2.9g/dL). U/A showed active sediments and nephrotic range proteinuria of about 4 g/ day. Proteinuria workup was done, including serologic workup. Labs were remarkable for elevated ESR (105), low C4 (12), normal C3 (95) and elevated RF (44). ANA, HIV, HCV, light chain ratio, cryoglobulins and ANCA were negative. UPIEP showed faint IgG kappa. CXR showed hazy interstitial opacities with a perihilar distribution. Pre-biopsy COVID molecular testing came back positive. He was diuresed aggressively and received losartan for BP control. A kidney biopsy was performed and revealed MPGN pattern with IF strongly positive for IgA in addition to weaker staining for C3, and IgG. EM showed subendothelial humps with few mesangial and subepithelial deposits. The diagnosis of IgA-dominant immune complex-mediated glomerulonephritis consistent with IRGN was made. Discussion: IGA-IRGN is a rare variant of IRGN that has been mostly associated with S. aureus infections. In this case, the recent COVID-19 infection in this patient could reasonably explain the finding of IGAD-IRGN on kidney biopsy. IGAD-COVIDrelated GN has been reported only once in the literature. Up until recently, most cases of COVID related kidney injury have been associated to ATN and collapsing FSGS. A immunohistochemistry test for COVID in kidney tissue was sent, which is pending at the time of this submission. If confirmed positive, this could be the second confirmed case COVID related IGAD-IRGN. It is important for nephrologists to include IGAD-IRGN in the differential diagnosis in a COVID patient with nephrotic syndrome. Renal Biopsy is of utmost importance for diagnosis.

Lupus nephritis presenting with positive PR3-ANCA and decreased ADAMTS13

Introduction: Lupus nephritis is a well-described entity. The simultaneous presence of ANCA abs is rare and is related to poor prognosis. Positive patients usually have MPOANCA. We present a case of biopsy-proven Class IV/V Lupus nephritis with PR3-ANCA and decreased ADAMTS 13 activity in an AA man. Case Description: This 46-year-old AA man with no known past medical history presented to the ED for two weeks of SOB, leg, and scrotal swelling. He denies any associated symptoms. He denies using any other OTC medications and illegal drugs. On exam, vital signs were stable. He had 2+ pitting edema in LE bilaterally, scrotal and penile edema. Other systems were unremarkable. Labs were significant for Hg 5.1, Platelets 106, K 6.9, CO2 9, BUN 78, Cr 10.2, and Albumin 2.4. UA showed dysmorphic RBCs and proteinuria, and Urine protein/creatinine of 9. COVID-19 testing was negative. HIV1&2, RPR titer, hepatitis panel, rheumatoid factor, ASO screen were all negative. Renal U/S showed normal-sized kidneys and no hydronephrosis. ANA, ANA titer, and anti-dsDNA returned elevated at >10,1:640 and 9.9IU, respectively. PR3-ANCA was also positive, but MPO-ANCA negative. C3 and C4 at 0.4g/L and 0.14g/L, respectively. ADAMTS-13 activity decreased to 40%. The rest of the work-up was negative. Kidney biopsy confirmed lupus nephritis, Class IV, and V, with ∼50% cellular crescents. Moderate to advanced interstitial fibrosis and tubular atrophy ∼50%. EM showed two globally sclerotic glomeruli. IF showed a full-house with IgG, IgA, C3, C1q, kappa, and lambda. Unfortunately, kidney function did not recover, and hemodialysis was started, and he was treated with MMF, Methylprednisolone, and with plasma exchange. Discussion: ANCA positivity, although not common, is a well-described entity but not understood in lupus nephritis patients. Most of these patients present with MPO-ANCA rather than PR3-ANCA. This subset of patients usually presents clinically differently with distinct histopathological features. Long-term follow-up in these patients is also needed to better understand this disease process in lupus nephritis patients.

Severe rhabdomyolysis in the time of coronavirus

Introduction: Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has become a global pandemic with alarming numbers of morbidity and mortality. COVID-19 primarily presents as a lung infection, with symptoms of fever, cough, myalgia, and fatigue. The severity of the disease may range from a mild upper respiratory infection to severe pneumonia, ARDS, and death. This novel disease can also present with involvement of multiple organ systems including the kidneys. Acute kidney injury (AKI) has been reported in up to 37 % of cases. Here we report a case of a woman with COVID-19 presenting with rhabdomyolysis and AKI. Case Description: A 48 y/o Hispanic woman with history of HTN, hyperlipidemia and DM type 2 who presented to the ED complaining of shortness of breath, fever, cough, and myalgias. Four days before presentation she had been diagnosed with COVID-19 and was self-isolating at home. Her symptoms worsened prompting her visit to the ED. Vital signs showed fever of 103.1 F, pulse 86, respirations 37, blood pressure 106/58 and O2 Sat 85% at room air, 95% with nasal canula at 4 L. PE was normal except for tachypnea and coarse breath sounds bilaterally on lung auscultation. Admission labs were remarkable for AKI and rhabdomyolysis. Serum creatinine was 3.61, BUN 83, and total CK 106,193. U/A with blood, 5-10 RBC, 5-10 WBC and many bacteria. FeNA was 0.3%. Toxicology panel was negative. Respiratory viral panel was negative. Influenza A and B are negative. She initially received 2 L bolus of IV NS and then continued with balanced crystalloid solutions for volume expansion over the next 3 days. She received treatment with hydroxychloroquine, azithromycin and ceftriaxone for COVID-19 pneumonia. Her symptoms improved and serum creatinine and CK gradually decreased until back to normal levels. Discussion: Rhabdomyolysis can be seen associated with viral infections. We presented a patient with COVID-19 and rhabdomyolysis. There are no studies establishing a mechanism for COVID-19 induced rhabdomyolysis. Patients with COVID-19 pneumonia are generally kept with negative fluid balance to avoid overload and worsening of ARDS. On the other hand, volume expansion is mainstay management for rhabdomyolysis. Clinicians should have a high suspicion for rhabdomyolysis in patients with COVID-19 presenting with myalgias and AKI. Early recognition of and appropriate treatment is crucial to improve outcomes.

Battling warburg: Type B lactic acidosis in a patient with diffuse large B-cell lymphoma

Introduction: The Warburg effect is a rare paraneoplastic syndrome seen in patients with hematologic malignancy. The metabolism of cancerous cells converts to aerobic glycolysis and results in type B lactic acidosis. Case Description: The patient is a 62-year-old man with diffuse large B-cell lymphoma and prior hemophagocytic syndrome (HS) diagnosed 6 months prior, on chemotherapy. He presented with several weeks of fever and respiratory symptoms. Clinical exam and diagnostics did not reveal a source of sepsis. Chest radiography and CT chest were without infiltrates. COVID-19 PCR was negative. Labs- WBC 1,500 /mm3, Hemoglobin 8.8 g/dL, Platelets 63,000 /mm3, creatinine 1.1 mg/dL, lactate 2.6 mmol/L, ferritin 417 ng/mL, serum triglycerides 349 mg/dL. Patient was placed on vancomycin and cefepime and volume expanded, but continued febrile with persistent lactic acidosis. Abdominal CT revealed splenomegaly with focal hypodensities, mild descending and sigmoid diverticulosis without diverticulitis. CT mesenteric angiography revealed moderate narrowing of celiac artery and severe narrowing of the inferior mesenteric artery origin. For suspected ischemic colitis, the patient was taken emergently for exploratory laparotomy, but findings did not support ischemia. Creatinine trended up to 2.0 mg/dL with increasing lactate of 11 mmol/L, bicarbonate 13 mmol/L, and serum pH of 7.0. At this point, without septic or ischemic processes identified, the lactate production was attributed to DLBCL, and not HS as ferritin was not substantially elevated. CRRT was initiated for anuric AKI. Lactate continued to trend up to 21.7 mmol/L with bicarbonate 6 mmol/L. Family discussions were held, and the patient was transitioned to palliative care. Discussion: Type B lactic acidosis should be considered in the differential diagnosis in patients with increased anion gap metabolic acidosis and malignancy. One rare and potentially fatal Type B lactic acidosis is due to the Warburg effect, a rare and potentially lethal paraneoplastic syndrome of hematologic malignancies.

Diagnosing vasculitis in the era of COVID-19: A diagnostic dilemma for house staff officers

Introduction: During our current pandemic, physicians must exclude COVID-19 in every patient presenting to the hospital with a febrile illness. However, every patient should have a complete work-up done to not miss other disease processes. Here we describe a case of microscopic polyangiitis with symptoms mimicking COVID-19. Case Description: The patient is a 69 yo female with history of HTN who presented with four weeks of polyarthralgia and fevers;this was accompanied by a dry cough and morning stiffness in her shoulders and hips, for which she heavily used ibuprofen. Vital signs were within normal limits. Physical exam showed clear breath sounds with 2+ pitting edema in the lower legs and no rashes. Labs reveled a WBC of 20,000 cells/ microliter, with creatinine of 2.29 mg/dL, bicarbonate of 17 mmol/L, and C-reactive peptide of 204 mg/L. UA showed moderate leukocyte esterase, trace protein, and large blood. Serum C3 and C4 levels were normal, and a spot urine/protein ratio was 600 mg. Urine microscopy had several non-dysmorphic RBCs with occasional RBC and WBC casts. Infectious work-up via COVID-19 screening, blood cultures, hepatitis, and HIV was negative. The patient's creatinine trended up, peaking at 2.8 mg/dL. She was started on empiric solumedrol at a dose of 60 mg TID for possibilities of polymyalgia rheumatica or vasculitis or NSAID-induced acute interstitial nephritis. She had a positive MPO ANCA with titer of 1:320. Kidney biopsy confirmed pauci-immune crescentic glomerulonephritis, with clinical diagnosis of microscopic polyangiitis. She was placed on prednisone 40 mg daily and rituximab 375 mg/m 2 weekly for four weeks and was discharged home in stable condition. Discussion: Systemic vasculitis remains to be a diagnostic challenge, especially in the era of COVID-19, given the overlap in symptoms. The diagnosis is made via clinical history and histopathological findings coupled with positive ANCA. Despite treatment, almost a quarter of these patients will progress to ESRD. In the era of COVID-19, great care must be taken to diagnose the kidney manifestations of systemic vasculitis.