{"title":"Improvement in proteinuria with sodium-glucose cotransporter 2 inhibitors and esaxerenone treatment in patients with chronic allograft kidney disease: A case report.","authors":"Shoichiro Daimon","doi":"10.5414/CNCS111078","DOIUrl":"10.5414/CNCS111078","url":null,"abstract":"<p><p>Proteinuria is a predictor of end-stage renal disease. The effectiveness of an angiotensin-converting enzyme inhibitor or an angiotensin II receptor blocker for the reduction in urinary protein excretion and renoprotection in proteinuric chronic kidney disease patients is well known, and coadministration of and sodium-glucose cotransporter inhibitor and the mineralocorticoid receptor blocker eplerenone has recently demonstrated an additive albuminuria-lowering effect in chronic kidney disease patients. Proteinuria is also an independent predictor of end-stage renal disease in kidney transplant recipients. Sodium-glucose cotransporter 2 inhibitors were administered to a 60-year-old man with chronic allograft kidney disease who had increasing urinary protein excretion with valsartan treatment. Although urinary protein excretion decreased drastically, it later increased to the same levels. A nonsteroidal mineralocorticoid receptor blocker, esaxerenone, was added to these medications, again resulting in a decrease in urinary protein excretion. Although the long-term renoprotective effect is not known, these medicines are promising and safe agents to reduce urinary protein excretion in patients with chronic allograft kidney disease.</p>","PeriodicalId":510898,"journal":{"name":"Clinical nephrology. Case studies","volume":"12 ","pages":"26-31"},"PeriodicalIF":0.0,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10955327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140186769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Massive acetaminophen ingestion managed successfully with N-acetylcysteine, fomepizole, and renal replacement therapy.","authors":"Elizabeth E Williams, Duc Quach, Arthur Daigh","doi":"10.5414/CNCS111275","DOIUrl":"10.5414/CNCS111275","url":null,"abstract":"<p><p>Acetaminophen ingestion is routinely managed with the antidote, N-acetylcysteine (NAC). Massive acetaminophen poisoning has been treated successfully with adjunctive therapies such as fomepizole and hemodialysis. Fomepizole functions by inhibiting cytochrome p560, which prevents tylenol from forming its toxic metabolite, NAPQI. Prior cases have demonstrated favorable outcomes and a significant drop in acetaminophen levels after a single session of intermittent hemodialysis and continuous veno-venous hemofiltration (CVVH). However, the recommended dosage adjustments of NAC and fomepizole while a patient is undergoing CVVH has not been well reported. We present a case of an 18-year-old male who presented after ingesting 125 g of tylenol. His 4-hour acetaminophen level was 738.6 µg/mL. He was treated with NAC, fomepizole, and a single 4-hour session of hemodialysis. His acetaminophen level remained elevated at 730 µg/mL despite the hemodialysis session. CVVH was initiated, and he was given intravenous NAC at 12.5 mg/kg/h, oral NAC at 70 mg/kg every 4 hours, and intravenous fomepizole at 10 mg/kg every 6 hours. His tylenol levels became undetectable 57 hours after ingestion, and he did not develop permanent liver toxicity. This case encourages the use of CVVH for massive tylenol ingestion when a single run of intermittent hemodialysis is not effective in lowering the tylenol level. NAC, fomepizole, and CVVH can prevent unfavorable outcomes in massive acetaminophen ingestion when provided at an appropriate dose and frequency.</p>","PeriodicalId":510898,"journal":{"name":"Clinical nephrology. Case studies","volume":"12 ","pages":"22-25"},"PeriodicalIF":0.0,"publicationDate":"2024-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10913534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140041226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pablo Rodríguez-Doyágüez, Motornaya-Morozova, Patricia Martínez-Miguel, Carolina Castillo-Torres, Óscar Toldos-González, Juan José Gil-Fernández
{"title":"Monoclonal gammopathy of renal significance: An atypical presentation of Waldenström's disease.","authors":"Pablo Rodríguez-Doyágüez, Motornaya-Morozova, Patricia Martínez-Miguel, Carolina Castillo-Torres, Óscar Toldos-González, Juan José Gil-Fernández","doi":"10.5414/CNCS111200","DOIUrl":"10.5414/CNCS111200","url":null,"abstract":"<p><p>Waldenström's disease is a rare lymphoproliferative syndrome in the bone marrow and sometimes in lymphoid organs which secretes high amounts of monoclonal immunoglobulin M into serum. It can remain indolent for years and rarely affects the kidney, with intraglomerular rather than intratubular damage being predominant, in contrast to multiple myeloma. Different studies identified AL amyloidosis as the most frequent renal lesion, followed by cryoglobulinemic glomerulonephritis. Signs and symptoms may be unspecific, as well as renal manifestations, so collaboration between nephrologists, hematologists, and pathologists is crucial to establish the role of paraprotein in the development of renal damage. We present an atypical case of Waldenström's disease that had a minimal monoclonal peak and clinically debuted with nephritic and nephrotic syndromes. The diagnosis was cryoglobulinemic glomerulonephritis. Currently, there are numerous treatment options, without enough evidence yet to establish a standardised treatment.</p>","PeriodicalId":510898,"journal":{"name":"Clinical nephrology. Case studies","volume":"12 ","pages":"17-21"},"PeriodicalIF":0.0,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10862989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139731451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Julie Bech Jensen, Eva Gravesen, Sidse Graff Jensen, Iain Bressendorff
{"title":"A case report of atypical anti-glomerular basement membrane nephritis associated with Mycobacterium Avium.","authors":"Julie Bech Jensen, Eva Gravesen, Sidse Graff Jensen, Iain Bressendorff","doi":"10.5414/CNCS111254","DOIUrl":"10.5414/CNCS111254","url":null,"abstract":"<p><p>We present the case of a woman with atypical anti-glomerular basement membrane (anti-GBM) nephritis associated with concurrent pulmonary infection with <i>Mycobacterium avium</i>. A kidney biopsy showed crescentic glomerulonephritis with 50% active crescents and linear IgG staining, but no circulating anti-GBM antibodies were detected, and the patient did not have pulmonary hemorrhage. Despite treatment with a triple-regimen of antibiotics, corticosteroids, and plasmapheresis, the patient did not regain kidney function. One year later she is on maintenance dialysis and has still not cleared the infection with <i>M. avium</i>.</p>","PeriodicalId":510898,"journal":{"name":"Clinical nephrology. Case studies","volume":"12 ","pages":"12-16"},"PeriodicalIF":0.0,"publicationDate":"2024-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10795487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139492399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Chelsea Guymer, Sadia Jahan, Bobak Bahrami, David Sia, Bee Qung Tan, Stephen McDonald, Sumu Simon
{"title":"Calciphylaxis, beware the ophthalmic mimic: A case series.","authors":"Chelsea Guymer, Sadia Jahan, Bobak Bahrami, David Sia, Bee Qung Tan, Stephen McDonald, Sumu Simon","doi":"10.5414/CNCS111088","DOIUrl":"10.5414/CNCS111088","url":null,"abstract":"<p><strong>Purpose: </strong>We present two atypical cases of calciphylaxis presenting with ocular ischemic pathology - both without the hallmark cutaneous manifestations - to raise awareness of this rare yet highly disabling condition.</p><p><strong>Observations: </strong>We report two cases of ophthalmic calciphylaxis presenting as (1) anterior ischemic optic neuropathy (AION) and cilioretinal artery occlusion in a 76-year-old woman with pre-dialysis kidney failure, and (2) AION with contralateral central retinal artery occlusion (CRAO) in a 44-year-old man on hemodialysis.</p><p><strong>Conclusion and importance: </strong>These cases highlight the need for judicious clinical suspicion of calciphylaxis in patients with kidney failure, presenting with microvascular ischemic ophthalmic pathology such as AION or CRAO. Confirmation with temporal artery biopsy is essential to direct targeted individualized multi-disciplinary treatment of calciphylaxis and avoid unnecessary steroid exposure in cases masquerading as giant cell arteritis (GCA).</p>","PeriodicalId":510898,"journal":{"name":"Clinical nephrology. Case studies","volume":"11 ","pages":"136-146"},"PeriodicalIF":0.0,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10759205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139089896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lina Bruns, Linus Völker, Robert Klamroth, Martin K Kuhlmann, Wolfram J Jabs
{"title":"Concomitant presentation of thrombotic thrombocytopenic purpura, immune thrombocytopenia, and autoimmune hemolytic anemia in a patient with newly diagnosed systemic lupus erythematosus.","authors":"Lina Bruns, Linus Völker, Robert Klamroth, Martin K Kuhlmann, Wolfram J Jabs","doi":"10.5414/CNCS111193","DOIUrl":"10.5414/CNCS111193","url":null,"abstract":"<p><p>Thrombocytopenia is always of concern when encountered in emergency settings. We report a case of a 29-year-old women in whom a unique constellation of hematological disorders occurred. The patient had been diagnosed with idiopathic immune thrombocytopenia (ITP) in 2007, with a history of several thrombocytopenic flares. She now presented with homonymous hemianopia accompanied by thrombocytopenia and microangiopathic hemolytic anemia (MAHA) and was soon after diagnosed with a posterior stroke. Symptoms were more reminiscent of acquired thrombotic thrombocytopenic purpura (aTTP) rather than ITP. Immediate treatment with plasma exchange and caplacizumab curtailed MAHA, and progressive ischemic disease was averted. ADAMTS-13 testing confirmed the diagnosis of immune-mediated aTTP. Repeated testing for ITP, however, also showed IgG-loaded thrombocytes with the former known anti-GPIIb/IIIa specificity. Furthermore, autoimmune hemolytic anemia (AIHA) could be detected by direct antiglobulin test showing IgG and complement loading of the patient's erythrocytes. The autoimmune background of all three entities suggested an underlying systemic disease. Indeed, systemic lupus erythematosus (SLE) serology was strongly positive allowing for the diagnosis of SLE. ITP and AIHA as well as aTTP can be secondary to SLE, but emergence of all three disorders has not been reported at the same time.</p>","PeriodicalId":510898,"journal":{"name":"Clinical nephrology. Case studies","volume":"11 ","pages":"147-153"},"PeriodicalIF":0.0,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10759207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139089897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}