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Introduction: The incidence of glomerular diseases varies across different countries and criteria for kidney biopsy has changed over time. In Uruguay, glomerular diseases (GD) are a frequent cause of end stage kidney disease (ESKD) and renal replacement therapy with an annual incidence of 25.0 patients per million population according to data from the Uruguayan Dialysis Registry (UDR, year 2020). Since 1970, the Uruguayan Registry of Glomerulopathies has been recording the incidence, epidemiology and evolution of patients with GP in our country. In 2018, the Glomerulopathies Biobank (GB) began to operate including all patients with a native kidney biopsy performed at the Nephrology Department of the teaching hospital Hospital de Clinicas in Montevideo, Uruguay. The purpose of the BG is to record the phenotype (clinical and paraclinical) of patients with GD diagnosed by renal biopsy and at the same time store blood, urine, renal tissue and DNA samples. The aim of this report is to communicate the first 110 patients enrolled in the BG, which started in February 2018. Method(s): The BG protocol includes the collection of patronymic data, personal history, and clinical and paraclinical features of renal pathology. Plasma, urine and cell samples are stored for subsequent DNA extraction at the time of the kidney biopsy. In our country, all renal biopsies are performed by nephrologists. The Glomerular Biobank project is funded by the Nephrology Research Fund (School of Medicine, University of the Repubic) and was approved by the Ethics Committee of the Hospital de Clinicas and the Regulatory Verification Unit of the National Institute of Donation and Transplantation. The results are presented as mean and standard deviation (SD) for the continuous variables;and qualitative variables are described with percentages. Result(s): Patient recruitment began in February 2018 and we have recruited 110 patients. The mean age at the time of biopsy was 38.3+/-16.1 (min:16;max:78) years. Regarding sex distribution, the female sex slightly predominated (55.3%). Plasma creatinine was 2.1+/-1.45 mg/dL, proteinuria was 3.1+/-3.7 gr/dL and albuminaemia was 3.2+/-1.0 mg/dL. Microhaematuria was present in 61% of patients in the sediment study. Figure 1 shows the negative impact of the COVID 19 pandemic on the incidence of patients undergoing kidney biopsy. IgA nephropathy (13,8%)was the most frequent primary glomerular disease, followed by d focal and segmental glomerulosclerosis and membranous nephropathy. Consernig the glomerulopathies secondary to a systemic disease, the most frequent diagnosis was lupus nephritis (34,5%) followed by vasculitis, amyloidosis and diabetes. Conclusion(s): Having a prospective cohort of patients with glomerular disease, including reliable data and biological samples, will allow us to perform clinical and epidemiological analyses quickly and reliably in the future. The data and aliquots of biological material are available to any local nephrologist who proposes a hypothesis and has the approval of the corresponding ethics committee. The medium-term objective is to incorporate other national reference institutions in the care of patients with glomerular diseases. The data collected by the Glomerular Biobank will be a valuable input to the process of continuous improvement, and will serve as a basis for future nephrological research of excellence. No conflict of interestCopyright © 2023
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Introduction: Membranous nephropathy is one of the most common causes of nephrotic syndrome. Among the available treatment options, the tried and tested regimen is the modified Ponticelli regimen. Despite adequate therapy, studies have shown that close to one-quarter of patients fail to attain complete remission. However, data is limited regarding patients who are resistant to this regimen. Method(s): This was an ambispective, observational study conducted in Madras Medical College, Chennai, India between April 2021 to August 2022. All patients with biopsy-proven primary membranous nephropathy resistant to modified Ponticelli regimen were included. Complete remission was defined as proteinuria < 0.5g/day combined with a stable eGFR. Partial remission was defined as reduction of proteinuria by 50% to < 3.5g/day but >0.5g/day. Resistance to therapy was defined as the failure to attain at least partial remission, 12 months after completion of modified Ponticelli regimen. Result(s): A total of 13 patients were enrolled in the study. The median age was 41 years (IQR 38-49) with a male preponderance (n=9;69%). Serum MPLA2R antibody was positive for 9 patients. All patients were negative for ANA and serology for hepatitis B, hepatitis C and HIV were negative. The most common clinical presentation was with nephrotic syndrome, seen in nine patients (69.23%). Renal failure was seen at presentation in 4 patients (30.76%), with one patient warranting initiation of hemodialysis. At 12 months, post completion of modified Ponticelli regimen, the median quantum of proteinuria was 8.7 grams per day. Due to trend towards normalisation of serum albumin and immunological remission, 3 patients were managed with optimised RAS inhibition after modified Ponticelli regimen. Currently, they are in partial remission. Four patients were treated with a second course of modified Ponticelli regimen. Of them one patient is in partial remission, while two patients had progressed to end-stage renal disease and are currently on maintenance hemodialysis. One patient who was resistant to the second course, was managed with a trial of calcineurin inhibitors (CNI) therapy followed by 4 doses of Rituximab (500mg each) due to persistent proteinuria. However, he was lost to follow up during the COVID pandemic and presented with end stage renal disease warranting hemodialysis. A trial of CNI therapy was given to 6 patients. All patients had nephrotic-range proteinuria 12 months post CNI therapy initiation. Five patients were then given Rituximab, among whom, two patients attained complete remission, while three patients have attained immunological and clinical remission. One patient was given a second trial of modified Ponticelli regimen following CNI therapy and is currently in complete remission. Two of these patients developed thrombotic complications - one patient diagnosed with coronary artery disease and one patient with renal vein thrombosis. Conclusion(s): Rituximab is a promising option for patients with primary membranous nephropathy who do not respond to modified Ponticelli regimen. No conflict of interestCopyright © 2023
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Background: Membranous nephropathy is a relatively common glomerular pathology that manifests with either nephrotic or sub-nephrotic range proteinuria. Evidence is emerging of COVID-19 and its vaccines having an influence on various glomerular diseases, including IgA nephropathy and minimal change disease, with limited information on membranous nephropathy. Data from our tertiary centre suggested a rise in cases of membranous nephropathy within a month after vaccination. Method(s): Patients who had renal biopsies in 2021 were identified from pathology results and online clinical records. Information on COVID-19 status, COVID vaccinations and biochemical results were compared. Patients were then split into 2 groups;those presenting within 1 month of vaccination or COVID infection and those who hadn't had vaccinations or a COVID infection within 4 weeks of presentation. Result(s): Complete vaccination and COVID infection history was present in 17 of the 24 patients. Of the 17 patients, 6 were in group 1 and 11 in group 2. 16 out of the 17 patients had nephrotic range proteinuria, 6 also had an AKI at presentation. There was no significant difference in presentation between the groups (see table 1). Conclusion(s): Our data has not conclusively shown a difference between the two groups probably because of the low numbers. But further studies are needed to see if there is a link between either COVID infections or COVID vaccinations and glomerular disease.
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The role of infectious agents derived antigens including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been recognized as a trigger for development of autoimmune mediated disorders following natural infection or immunization. However, there is a scarcity of reports of occurrence of autoimmune associated kidney disorders or flare ups following exposure to a SARS-CoV-2 vaccine. A 65-year-old female presented to a nephrology clinic for evaluation of worsening renal dysfunction. The patient is well known to have systemic sarcoidosis under complete remission on low dose prednisone and likely membranous nephropathy (no previous kidney biopsy) with mildly elevated phospholipase A2 receptor (PLA2R) antibodies. Her membranous nephropathy was in partial remission on angiotensin receptor blockage, with urine to protein creatinine ratio (UPCR) of 1.5 g/g . Five months after receiving the single dose SARS-CoV-2 vaccine (Johnson & Johnson®), she started having a flare up of her systemic sarcoidosis with worsening joint, skin and respiratory symptoms. Blood chemistry revealed worsening renal dysfunction with elevated creatinine up to 1.7 mg/dL from her baseline of 1.0 mg/dL. UPCR was also elevated at 3.4 g/g. Urine sediment revealed no red blood cells or casts, only several calcium oxalate dihydrate crystals. A kidney biopsy was performed and showed a combination of membranous nephropathy (PLA2R positive) along with granulomatous interstitial nephritis with well-formed epithelioid granulomas characteristic of sarcoidosis. She was started on high dose prednisone and her renal function improved to 1.2 mg/dL, UPCR decreased to 1.8 g/g and serum PLA2R antibodies became undetectable. She is still being monitored. After many years of renal sarcoidosis and membranous nephropathy remission, the relapse of renal disease after receiving the SARS-CoV-2 vaccine (Johnson & Johnson®) suggests the association between receiving the vaccine and the recurrence of renal sarcoidosis and membranous nephropathy.
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BACKGROUND AND AIMS: The mass vaccination for COVID-19 has raised new concerns for patients with immune-mediated nephropathies: there is a small but growing literature of case-reports linking SARS-CoV-2 vaccines with heightened off-target immune responses leading to De novo or relapsing glomerular diseases [1, 2]. Aim of this study was to evaluate how many and how severe were the relapses of immune-mediated nephropathies after the SARS-CoV-2 vaccine in a single center. METHOD: This is a retrospective study held in Italy from the start of the vaccination campaign (late December 2020) to December 31st 2021. We included all patients with an immune-mediated nephropathy (either on or off immunosuppressive therapy-IS), excluding patients with an end-stage renal disease or kidney transplant. In Italy we used mRNA (Comirnaty by Pfizer-BioNTech or Spikevax by Moderna) or adenoviral vector vaccines (Vaxzevria by AstraZeneca or Janssen), without any preference for patients with kidney disease, but those on active IS were given preferentially an mRNA vaccine. There was no active surveillance of lab tests after vaccination and post-vaccine tests were either concomitant to programmed visits or suggested on a patient by patient basis. Recurrence was defined as relapse of nephrotic or nephritic syndrome, doubling of urinary proteins with a max value > 1 g/24h, acute kidney injury with an active urinary sediment, or positivization or 5-fold increase of serological markers of disease activity (i.e.: ANCA in AAV). RESULTS: A total of 38 patients (M: F 28:10, age at vaccine 45.9 ± 19.1 years) completed the vaccination protocol: among them, the most common nephropathy was membranous nephropathy (n = 12, 31.6%), followed by IgA nephropathy (n = 7, 18.4%), minimal change disease (n = 6, 15.8%) and ANCA-associated vasculitis (n = 6, 15.8%);26 patients (68.4%) had at least one other comorbidity. We observed six relapses (4 MN, 1 IgA, 1 AAV), of which only one (MN) developed a mild oedema. The mean time from the first vaccine dose to the relapse was 101 ± 71 days (5-199 days) and only two episodes occurred within 4 weeks from a vaccine dose. We could not find an association between recurrences and maintenance IS at the time of vaccine or any other variable. The overall post-vaccine incidence rate of relapses was 35.8/100 patient-years, as compared with 14.0/100 patient-years historically observed in the same cohort [IRR 2.55, 95% confidence interval (CI) 0.89-5.97]. CONCLUSION: Relapses of immune-mediated nephropathies are not common after SARS-CoV-2 vaccine and we did not observe any clinically relevant relapse. However the overall rate of relapse seems to be a little higher than prior vaccination [3], but only 2/6 patients recurred soon after a vaccine dose. As these relapses seem to be self-limiting, a post-vaccine monitoring could be useful in patients at high risk of severe disease.
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BACKGROUND AND AIMS: In the COVID 19 pandemic era, anti SARS-CoV-2 vaccination showed high efficacy at preventing the infection and its most severe complications. The aim of this report is to describe an unusual double glomerulopathy related to anti SARS-CoV-2 vaccination and the good results obtained with the immunosoppressive treatment. METHOD: An 80-year-old caucasian woman developed a nephrotic syndrome, progressive renal insufficiency and microhematuria. The patient presented a medical history of thrombocytopenic purpura treated and resolved by steroids in 2013, hypothyroidism, hypertension, ischaemic heart disease treated with surgical bypass in 2019 and pacemaker in 2020 for atrial ventricular block. Due to pandemic COVID 19 status, she received two doses of the Pfizer BioNTech mRNA COVID-19 vaccine in March 2021. Two weeks after the second dose her weight increased of 23 kg. The family physician added furosemide to her therapy for generalized edema with no diuretic effect. In April, creatinine was 1.38 mg/dL (versus 0.8 mg/dL 1 year before);urinalysis showed proteinuria (300 mg/dL) and microscopic hematuria;serum total cholesterol level was 218 mg/dL and triglycerides 178 mg/dL;then it was suggested to increase the doses of furosemide. In May 2021, creatinine resulted 2 mg/dL, serum albumin 2 g/dL, and urinalysis confirmed proteinuria and microscopic hematuria;proteinuria was 10 g/day. Abdomen ultrasound showed normal liver, kidneys and spleen, not ascites. Lower limb eco-Doppler showed right superficial femoral artery stenosis of 60% and absence of venous thrombosis. The physical examination evidenced anasarca. The patients were admitted to the nephrology unit;hepatitis B surface antigen, hepatitis C antibody and human immunodeficiency virus antigen and antibody were negative. Both complement C3 and C4 levels resulted within the normal range. Cryoglobulins were absent. Urinary Bence Jones, antinuclear antibody (ANA), anti-extractable nuclear antigen (ENA), anti-double stranded DNA (nDNA) antibodies were negative. Antineutrophil cytoplasm antibodies (ANCA) were 1:2560 with Perinuclear pattern and anti-MPO positivity (716 UA/mL);anti-proteinase-3 antibodies (PR3) were negative. Antiphosholipase A2 receptor antibody (PLA2R Ab) was positive with high titre. A kidney biopsy was performed showing a double nephropathy: a focal segmental glomerulosclerosis (FSGS) with some collapsing features, superimposed on membranous glomerulonephritis (Fig. 1). RESULTS: We started the Ponticelli regimen (alternate months steroids and cyclophosphamide). After the first month of therapy, blood tests revealed creatinine 1.7 mg/dL, haemoglobin 11.7 g/dL;serum albumin 2.7 g/dL and urinalysis without microscopic haematuria. At the third month of therapy, the patient developed atrial fibrillation and started anticoagulation;blood tests were as follows: creatinine 1.1 mg/dL, serum albumin 3.0 g/dL, Ab anti-MPO 7 UA/mL and PLA2R Ab was absent. A left ocular, frontal and parietal herpes zoster induced a short discontinuation of therapy and responded well to Acyclovir;then we concluded the fourth month of therapy. At the fifth month, a SARS CoV 2 RT PCR unexpectedly resulted positive;the patient remained asymptomatic, but we stopped definitively the therapy. One month later, blood tests showed: creatinine 1 mg/dL, serum albumin 4 g/dL, proteinuria 0.7 g/die, MPO 2 UA/mL and PLA2R Ab absent. CONCLUSION: To our knowledge, this is the first case of nephrotic sindrome secondary to a De novo MN and FSGS, associated with positive MPO antibody, following Pfizer-BioNTech mRNA vaccination COVID 19;the patient responded well to immunosoppression going in remission and regaining renal function. (Figure Presented).
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BACKGROUND AND AIMS: The development and massive use of mRNA COVID- 19 vaccine BNT162b2 has raised new concerns on triggering De novo immunemediated diseases, in particular rare diseases as glomerulonephritis (GN), even if the security profile is excellent and severe reactions have been rare. In literature few similar cases were recently described [1, 2]. We report six cases of newly diagnosed GN after a two-dose regimen of SARS-CoV-2 vaccine, from a single tertiary care institution in Northern Italy. METHOD: We described six cases of De novo GN occurring after massive use of Pfizer-BioNTech BNT162b2 COVID-19 vaccine from March 2021 to December 2021. All cases were biopsy proven. Baseline characteristics and laboratory findings, treatments and outcomes were based on review of medical records. RESULTS: From April 2021, we observed two IgA nephropathies (IgA-N), one membranous nephropathy (MN), one membranoprolipherative GN (MPGN), one acute interstitial nephritis (aTIN) and one minimal change disease (MCD). Of note, one IgA-N presented with diffuse purpura as in IgA-vasculitis. The median age at vaccination was 52.8 years (min-max 18-67) and three (50%) were female;arterial hypertension was the most common comorbidity (50%). Only one subject contracted COVID-19 before vaccine (16.6%). None of the points showed any sign of renal disease before vaccine;at the time of disease onset, the median creatinine was 1.49 mg/dL (min-max 0.6-10.5 mg/dL) and proteinuria 3.0 g/24 h (min-max 0.9-13.8 g/24 h). All cases presented after the second dose (1 day to 6 months thereafter) and three (50%) were within 3 weeks from the vaccine. Of note, the aTIN developed after the vaccine during a long-time therapy with statins and relapsed after a rechallenge with a statin few months later. All the nephropathies were treated as per center practice, with an overall good response (four partial remissions and one complete remission). Given a target population of about 100 000-200 000 residents in our area, we could estimate an incidence rate of 4-8 cases/100 000 patient-years. CONCLUSION: This small series has a lot of limitations including the small number of patients and we probably missed some cases in our area. Furthermore, we could not investigate a causal association, even if the timing of disease onset might be suspicious in three cases and the incidence seemed to be almost twice as the expected in Europe (about 2-4/100.000 patient-years). As for SARS-CoV-2 vaccines, it is likely that the mRNA vaccine will result in a more potent inflammatory stimulus than the one observed after inactivated virus-vaccine: maybe some patients had already a subclinical GN and the vaccine constituted a flare leading to the full-blown disease [3].
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Case Report Background COVID-19 infection and COVID-19 mRNA vaccines have been associated with the occurrence of de-novo and relapsing glomerulopathies. Although, Focal Segmental Glomerulosclerosis (FSGS) similar HIV associated Nephropathy (HIVAN) has been reported with COVID-19 infection in African American population with Apolipoprotein L1 gene mutation, amongst the few reported cases post-vaccine, Minimal change disease (MCD), IgA nephropathy (IgAN), Anti-Glomerular basement membrane glomerulonephritis (Anti GBM GN), and membranous glomerulonephritis (MGN) have been reported. Case A 26-year-old Caucasian male with a history of tobacco use complained of Frothy urine and edema for 3 weeks post second dose of Moderna COVID-19 vaccine on 06/01/21. He received the first dose on 5/04/21. On his annual wellness visit on 5/18/21, he had no complaints, normal physical examination with serum albumin 5g/dl, and urinalysis significant for trace proteinuria. A repeat urinalysis post-onset of symptoms on 7/18/21 revealed 3+ proteinuria, no RBCs, 24- hour urine revealed 3.2g proteinuria. Further investigations revealed Hypoalbuminemia (2g/dl), persistent proteinuria, and an unremarkable renal ultrasound, ANA, ANCA, Anti-dsDNA, Anti-PLA2R, anti-streptolysin, RF, HIV, hepatitis panel, and serum complement levels. Renal biopsy revealed Tip lesion variant of FSGS with 100% effacement of podocyte foot process. Therapy with Prednisone 60 mg daily was initiated, following which an improvement in edema and serum albumin levels (2.7 g/dl) were noted. Discussion A few de-novo cases of anti-GBM GN, ANCA positive vasculitis, MCD and IgAN, and relapsing cases of IgAN, MCD, MGN, and Thrombotic microangiopathy have been reported post-COVID 19 mRNA vaccination. Most reported cases of MCD occurred after the first dose whereas IgAN flare-up occurred after the second dose. Our case is unique as our Caucasian patient developed FSGS post-second dose of Moderna vaccine. Although the pathogenesis is unclear, it is thought to be related to an acute T-cell immune response involving cytokine production to COVID 19 spike protein which is responsible for inducing or worsening existing podocytopathies. Interestingly fewer cases have been reported following adenovirus vector or inactivated virus vaccination. Most of the reported cases of IgAN flare-up have been mild and a small number of MCN cases required ICU admission for management of fluid overload. As observed in a few prior case reports our patient had a slow response to steroid therapy. Although guidelines on COVID 19 vaccination in patients with existing glomerulopathies remain unclear and are based on case-by-case scenarios, the benefit of COVID 19 vaccination, may in general, outweighs the risk of glomerular diseases. We encourage further studies on this topic, especially in the era of booster doses with ongoing discussion about mixing two types of vaccines.
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A 56-year-old male patient with a medical history of essential hypertension was referred to the emergency room after he was found to have a serum creatinine level of 13 mg/dL at his primary care physician's office. The patient reported that he had developed a coronavirus disease 2019 (COVID-19)-like infection six months prior that was not confirmed. Two months later, he started to notice dyspnea on exertion and bilateral lower limb swelling and was started on furosemide. He received the first dose of the Moderna COVID-19 vaccine a month before the presentation but did not receive the second dose. Subsequently, his lower limb swelling and exertional dyspnea started worsening. He denied any new medication, dysuria, oliguria, hematuria, fever, or any other symptoms. Initial evaluation was consistent with kidney failure. Hypocalcemia and hyperphosphatemia were noted, along with medical renal disease on renal ultrasound. Eosinophils and nephrotic-range proteinuria were found in the urine. His serum phospholipase A2 receptor (PLA2R) antibodies were positive. A renal biopsy showed membranous glomerulonephritis with moderate segmental sclerosis, as well as tubulointerstitial fibrosis with neutrophils, consistent with acute interstitial nephritis. Positive staining for PLA2R in the glomerular deposits suggested primary membranous nephropathy (MN). He was treated with prednisone first, and when the kidney biopsy was conclusive for membranous glomerulopathy, he was started on rituximab. On admission, he received hemodialysis intermittently, but this was stopped a month after discharge as his renal function normalized. Recently, there have been numerous cases reported with new onset of glomerular disease after receiving the COVID-19 vaccine. Further studies of vaccinated patients are needed to determine whether the severe acute respiratory syndrome coronavirus 2 virus vaccination is associated with a higher risk of MN and to identify potential predisposing factors and mechanisms of kidney injury in patients in whom it occurs.
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Case Report The purpose of this study is to describe a case study of possible glycosuria-induced hypernatremia in a patient hospitalized with COVID-19 acute respiratory distress syndrome. Methods Used Case study and literature review Summary of Results A 55-year-old man with a past medical history of non-insulin-dependent type II diabetes and hypertension developed hypernatremia, glycosuria, and acute kidney injury in the setting of COVID-19 pneumonia after resolution of diabetic ketoacidosis. The patient was initially admitted with a positive SARS-COVID-19 screening, a creatinine of 1.1 mg/dL (0.5-1.2) with glycosuria, and sodium of 137 mmol/L (136-145). Seventeen days into his hospital admission for severe acute respiratory distress syndrome, he developed hypernatremia (147 mmol/L). Over the subsequent twenty-two days, the patient continued to have hypernatremia up to 153 mmol/L refractory to treatment. In addition, the patient had persistent glycosuria and an elevated creatinine of 2.3 mg/dL (greater than thirty percent above his baseline). His total fluid balance was +1444 mL during this phase of hospitalization. The patient's electrolyte derangements concomitant with his worsening renal function suggests possible Fanconi syndrome. We hypothesize this is secondary to COVID-19. Conclusion COVID-19 has been shown to be associated with renal dysfunction, including acute tubular injury, such as membranous nephropathy and Fanconi syndrome. Experimental data have suggested that COVID-19 can infect renal proximal tubular cells via the Angiotensin Converting Enzyme 2 with subsequent development of incomplete Fanconi syndrome preceding acute kidney injury. Studies have also shown that glycosuria, proteinuria, pyuria, and hematuria may occur with COVID-19 regardless of comorbidities. We concluded our patient developed refractory hypernatremia secondary to glycosuria induced incomplete Fanconi syndrome due to COVID- 19.
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Introduction: Minimal change disease (MCD) is a major cause of idiopathic nephrotic syndrome (NS) which is composed of heavy proteinuria, hypoalbuminemia, and edema. It represents 15% of idiopathic NS in adults and the proportion of cases decreases with age as other entities such as membranous nephropathy become more common. Kidney damage associated with Toxicodendron species toxicity is quite rare but there are three lesions already described: proliferative glomerulonephritis, arteritis and membranous nephropathy. Here we report a case of MCD associated to Toxicodendron toxicity. Methods: A 47 year old mexican woman with no history of chronic diseases was referred to the nephrology office. She has a positive familiar history for diabetes and hypertension and she was recently vaccinated for COVID-19. She was referred for proteinuria incidentally found during routine tests three months ago which has been persistent on urinary testing afterwards, she recalls a Toxicodendron spp (poison ivy) exposure which led to an self-limited dermatitis 5 days before the first urinary test was taken. Initial workup showed 3.54 gr/24h proteinuria, hypoalbuminemia (3.2 gr/L) and hypercholesterolemia (256 mg/dl) and a nephrotic syndrome diagnosis was made. Further testing included negative HIV, HCV and HBV serology, normal C3 and C4 levels and negative anti-PLA2R, P-ANCA, C-ANCA, antinuclear antibodies. Normal kidneys were visualized on ultrasound. A kidney biopsy was performed and reported a minimal change disease. Steroid glucocorticoids was administered with methylprednisolone for three days and she was discharged with oral glucocorticoid for maintenance. On ambulatory follow up the patient had a dramatic improvement of the proteinuria. Results: A 47 year old woman developed proteinuria a few days after ivy poison exposure with a subsequent nephrotic syndrome. Renal biopsy shows a minimal change disease and good glucocorticoid response was met. Conclusions: Our hypothesis is that ivy poison exposure is directly involved in MCD onset in this patient. No conflict of interest
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Background: Nephrotic syndrome is known to be associated with hypercoagulable status. Pulmonary artery thromboembolism is one of the life- threatening complications in patients with nephrotic syndrome but rarely occurs before the diagnosis of nephrotic syndrome. Methods and Results: A 33-year-old man without any co-morbidities presented to a primary care clinic with sudden onset shortness of breath. An electrocardiogram showed sinus tachycardia with S1Q3T3. ECHO and CTPA revealed thrombi of the bilateral pulmonary arteries and he was COVID-19 negative by PCR analysis. Anticoagulant therapy was initiated immediately. Hypercoagulability workup showed normal levels of protein C, protein S, and AT III. He was ANA- and APLA negative and his homocysteine levels were normal. Lower limb Doppler showed multiple deep venous system thrombi. Three months following this episode, he presented with recurrence of acute worsening of breathlessness with pedal edema and abdominal distention. He was referred to our Cardiology emergency care. 2D Echocardiography showed classic Mc Connells sign with akinesia of RV free wall and RV systolic pressure of 60 mm Hg. CT pulmonary angiography definitively proved fresh (recurrence of) pulmonary embolism with large clots in both LPA and RPA and CXR showed classical signs of pulmonary embolism (Fig. 1). USG abdomen showed ascites, normal kidneys and no renal vein thrombosis. Laboratory examination showed he was COVID-19 negative again by PCR analysis. They also revealed low serum albumin (2.2g/dl) and nephrotic-range proteinuria (>10 gm in 24 hours) with transudative ascitic fluid. Since patient was on anticoagulation renal biopsy was deferred by the consultant nephrologist in view of possible bleeding complications. In view of possible primary membranous nephropathy, Serum Anti-Pla2r antibody was done which was strongly positive. The constellation of nephrotic-range proteinuria, pulmonary thromboembolic complications and associated serum anti-Pla2R antibody suggested primary membranous nephropathy. Immunosuppression was started as per modified Ponticelli regimen. Proteinuria resolved after three weeks and patient continues to be doing well on anticoagulation on oral VKA [Formula presented] Conclusion: Previous case reports of pulmonary artery thromboembolism associated with nephrotic syndrome are very few, particularly in adults. In the rare cases where they do occur, the patients initially present with the symptoms derived from nephrotic syndrome, unlike in our patient where the presentation was extremely rare and the investigation of the thromboembolic event led us “backwards” to the diagnosis of nephrotic syndrome. Awareness regarding the potential complications of hypercoagulable in nephrotic syndrome is thus essential.