Case Reports in Nephrology and Dialysis最新文献

{"title":"Deploying an FcMBL-Based Extracorporeal Blood Purification Filter in a Critically Ill Patient with COVID-19.","authors":"Conor Higgins, Samuel Ostrowski, Linda Barr, Bethany Radin, George Downey, Michael T McCurdy","doi":"10.1159/000549021","DOIUrl":"10.1159/000549021","url":null,"abstract":"<p><strong>Introduction: </strong>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of COVID-19, can progress to life-threatening disease and multiorgan failure, and the degree of circulating SARS-CoV-2 directly correlates to clinical deterioration and mortality. The engineered FcMBL protein binds numerous pathogens, including SARS-CoV-2, and pathogenic debris known as pathogen-associated molecular patterns (PAMPs).</p><p><strong>Case presentation: </strong>We report the first clinical use of an extracorporeal filter utilizing FcMBL to bind and remove pathogens and PAMPs from the circulation of a critically ill patient with COVID-19-induced multiorgan failure.</p><p><strong>Conclusion: </strong>This case highlights the feasibility of using the novel filter to reduce the circulating pathogen load in patients with severe infection through the use of agnostic pathogen binding via FcMBL.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"252-259"},"PeriodicalIF":0.9,"publicationDate":"2025-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12659594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145647366","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":"Management of Severe Hypercalcemia with Continuous Venovenous Hemodialysis and Regional Citrate Anticoagulation: A Case Report.","authors":"Ruben M F Hendriks, Charlotte van Noord, Marjolein F Looije","doi":"10.1159/000548630","DOIUrl":"10.1159/000548630","url":null,"abstract":"<p><strong>Introduction: </strong>Severe hypercalcemia is a potentially life-threatening condition that often requires urgent medical intervention, especially when refractory to conventional treatments. Continuous renal replacement therapy (CRRT) with regional citrate anticoagulation (RCA) is a therapeutic option, although data on its use in hypercalcemia are limited.</p><p><strong>Case presentation: </strong>We report the case of a 78-year-old woman who presented with severe hypercalcemia (4.89 mmol/L, corrected for albumin), ECG changes, muscle weakness, and acute kidney injury. She was unresponsive to standard treatments including crystalloids, diuretics, calcitonin, and bisphosphonates. Imaging revealed multiple lytic bone lesions and a mediastinal mass, with biopsy confirming diffuse large B-cell lymphoma. Continuous venovenous hemodialysis (CVVHD) with RCA was initiated after other therapies failed to lower calcium levels and symptoms persisted. Initial challenges with anticoagulation were resolved by increasing the citrate dose, along with an adapted calcium supplementation rate, leading to successful normalization of calcium levels within 30 h. Careful monitoring of post-filter calcium, systemic calcium and total-to-ionized calcium ratios, along with rapid dose adjustments, prevented complications such as hypocalcemia, citrate accumulation, and rebound hypercalcemia. The patient's calcium levels stabilized and she was transferred to a regular nursing ward to start oncological treatment.</p><p><strong>Conclusion: </strong>This case highlights the effectiveness of CVVHD with RCA in managing refractory hypercalcemia and underscores the importance of vigilant monitoring and individualized adjustments to prevent treatment-related complications.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"245-251"},"PeriodicalIF":0.9,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12618022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145538973","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":"Diffuse Cortical Necrosis of Native Kidneys in Sickle Cell Trait: A Case Report.","authors":"Basil Alnasrallah, Manaf Aljishi, Osama Alkhamees, Jafar Alrubh, Abdullah Alqawain, Shatha Alfaraj, Husam Alzayer","doi":"10.1159/000548631","DOIUrl":"10.1159/000548631","url":null,"abstract":"<p><strong>Introduction: </strong>Sickle cell disorders are the most common hereditary hematological disorders; sickle cell trait (SCT) is largely benign with mild clinical manifestations, if any. Renal cortical necrosis (RCN) is a rare and severe form of kidney injury and, to our knowledge, has not been previously reported to affect the native kidneys of patients with SCT.</p><p><strong>Case presentation: </strong>We describe a case of a 41-year-old male with a background of SCT who presented with acute abdominal pain and lower abdominal tenderness. He had rapidly rising creatinine over 48 h from 229 to 526 µmol/L, as well as elevated lactate dehydrogenase and total bilirubin at 2,606 U/L and 31 µmol/L, respectively. His toxicology, viral, and autoimmune profiles were negative, with a normal kidney ultrasound scan. The kidney biopsy revealed diffuse RCN. The patient was managed conservatively and had partial recovery of his kidney function to a baseline creatinine of 176 µmol/L 6 months later.</p><p><strong>Conclusion: </strong>Although SCT has long been considered a benign condition, growing evidence suggests that vaso-occlusive manifestations can occur, especially in the context of physiological stressors. This is the first described case of diffuse RCN affecting the native kidneys of a patient with SCT without an identifiable stressor, highlighting the need for vigilance in managing SCT and its potential severe kidney manifestations.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"238-244"},"PeriodicalIF":0.9,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12659409/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145647339","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":"Multiple Unilateral Subcapsular Cortical Hemorrhagic Cystic in the Left Kidney Disease: A Case Report of a Potential New Clinical Entity in Young Adults.","authors":"Luciano Wolffenbüttel, Renata Asnis Schuchmann, Gabriel Sartori Pacini, Pedro Guimarães Pascoal, Mateus Guimarães Pascoal, Gustavo Gomes Thomé, Elvino Barros","doi":"10.1159/000548647","DOIUrl":"10.1159/000548647","url":null,"abstract":"<p><strong>Introduction: </strong>Unilateral renal polycystic disease is a rare condition, first described in 1964, with over 60 cases reported worldwide. In 2019, Yoshida et al. [Eur Radiol. 2019;29(9):4843-50] identified 14 patients with unilateral renal cysts, who exhibited distinctive clinical and radiological features: young adults with multiple unilateral subcapsular cortical hemorrhagic (MUCH) cysts in the left kidney. The epidemiology, etiology, clinical significance, and prognosis of this condition remain largely unknown.</p><p><strong>Case presentation: </strong>We report a 36-year-old male who presented with nephrotic syndrome, generalized edema, and impaired renal function, requiring renal replacement therapy. Magnetic resonance imaging revealed unilateral subcapsular hemorrhagic cysts in the left kidney, with nearly normal renal size. A percutaneous biopsy of the right kidney showed acute tubular necrosis and focal segmental glomerulosclerosis, tip lesion variant. The patient achieved complete remission shortly after initiating immunosuppressive therapy, with full recovery of renal function. Whole exome sequencing did not reveal any pathogenic variants. A 99Tcm-DMSA scintigraphy, performed 20 months after the initial presentation, showed a renal uptake of 11.3% (reference range: 30 ± 6%) in the affected kidney, with normal uptake in the right kidney.</p><p><strong>Conclusion: </strong>MUCH cysts in the left kidney, observed in young adults, may represent a novel clinical entity. However, the epidemiology, etiology, clinical implications, and prognosis of this condition remain to be fully elucidated.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"231-237"},"PeriodicalIF":0.9,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12659407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145647411","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":"A Complement Factor B Mutation in a Chinese Family with Atypical Hemolytic Uremic Syndrome: A Case Report and Systematic Review.","authors":"Wan Peng, Xicui Long, Haoran Lei, Fengxiao Bu, Huijun Yuan, Yu Lu","doi":"10.1159/000547975","DOIUrl":"10.1159/000547975","url":null,"abstract":"<p><strong>Introduction: </strong>Atypical hemolytic uremic syndrome (aHUS) is a rare and potentially life-threatening condition, often linked to dysregulation of the complement system.</p><p><strong>Case presentation: </strong>In this study, a novel heterozygous <i>CFB</i> mutation was identified in both the index patient and her sister, who both developed aHUS following respiratory infections. While the index patient succumbed to the condition, her sister achieved remission following treatment with eculizumab. Interestingly, other family members carrying the mutation remained asymptomatic, illustrating intrafamilial variability.</p><p><strong>Conclusion: </strong>This study provides valuable insights for genetic counseling, prenatal diagnosis, and potential therapeutic strategies for aHUS patients with <i>CFB</i> mutations.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"224-230"},"PeriodicalIF":0.9,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249934","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":"Novel OFD1 Mutation Results in Unusually Early-Onset Polycystic Kidney Disease.","authors":"Nicholas Jones, Matthew Nguyen, Dao Le, Ramy Hanna","doi":"10.1159/000547878","DOIUrl":"10.1159/000547878","url":null,"abstract":"<p><strong>Introduction: </strong>Mutations of the OFD1 gene cause oral-facial-digital syndrome type 1 (OFD 1) and variations of the related ciliopathies Joubert syndrome and primary ciliary dyskinesia. OFD 1 manifests with skeletal, CNS, and renal abnormalities with prevalence estimated between 1 in 50,000 and 1 in 250,000. Cilia help regulate responses to mechanical forces in the renal tubules, and polycystic kidney disease (PKD) resulting from defective cilia is the primary determinant of morbidity in OFD 1. PKD associated with OFD 1 is rare before adulthood but may increase markedly with age, progressing to end-stage renal disease (ESRD) in 80% of cases.</p><p><strong>Case presentation: </strong>We report an 18-year-old female with congenital ciliopathy presenting with declining renal function and an increase of serum creatinine to 1.7 mg/dL. A 24-h urine collection yielded 0.8 g of creatinine and 500 mg of total protein. Imaging was conducted and genetic studies were repeated as her early childhood results were not available. MRI revealed numerous bilateral renal cysts consistent with progression of ciliopathy-associated PKD. Genetic testing confirmed the presence of a novel c.1332del frameshift mutation in the OFD1 gene, prematurely truncating the OFD1 protein. Modifications to diet and hydration to preserve renal function and delay progression to ESRD were initiated.</p><p><strong>Conclusion: </strong>This case of unusually early renal decline highlights the challenge of treating OFD 1. There are no currently approved medications and management consists of supportive measures to delay progression. Further research to better characterize and identify treatments for OFD 1 and related ciliopathies is warranted.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"216-223"},"PeriodicalIF":0.9,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249954","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":"A Case of Chronic Active T-Cell-Mediated Rejection Caused by Plasma Cell-Rich Acute Rejection 12 Years after Kidney Transplantation.","authors":"Ayaka Hayashi, Izumi Yamamoto, Mayuko Kawabe, Yutaro Ohki, Akimitsu Kobayashi, Fumihiko Urabe, Takafumi Yanagisawa, Shunsuke Tsuzuki, Jun Miki, Takahiro Kimura, Ichiro Ohkido, Nobuo Tsuboi, Hiroyasu Yamamoto, Takashi Yokoo","doi":"10.1159/000547828","DOIUrl":"10.1159/000547828","url":null,"abstract":"<p><strong>Introduction: </strong>Plasma cell rich-acute rejection (PCAR) is a variant of T-cell-mediated rejection in kidney transplantation. Its pathogenesis remains unknown and it is often refractory to standard immunosuppression strategies, possibly leading to allograft loss. Here, we report a case of chronic active T-cell-mediated rejection caused by PCAR 12 years after kidney transplantation.</p><p><strong>Case presentation: </strong>A patient first visited our outpatient clinic with hematuria and proteinuria at the age of 23. He was followed as an outpatient for suspected chronic glomerulonephritis, but his kidney function gradually deteriorated and hemodialysis was initiated at age 50. ABO-compatible kidney transplantation was performed at 51. His graft function was stable for 11 years post-transplant with a serum level of creatinine of 1.5 mg/dL. Twelve years post-transplant, however, his graft function worsened to a creatinine level of 3.2 mg/dL, and he was admitted to our hospital for an allograft biopsy. The histopathology showed edematous lesions with massive tubulointerstitial plasma cell infiltration, and severe tubulitis, consistent with chronic active T-cell-mediated rejection type 1B according to the Banff classification 2019. He was treated with steroid pulse therapy (methylprednisolone 1,000 mg for 3 consecutive days), and his graft function improved to a creatinine level of 2.2 mg/dL. A repeat allograft biopsy 3 months after the steroid therapy showed improved interstitial edema and tubulitis.</p><p><strong>Conclusion: </strong>As suggested in this case, it is still possible to achieve a favorable response by initiating appropriate treatment in early stages of PCAR.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"206-215"},"PeriodicalIF":0.9,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249907","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":"Nephritis-Associated Plasmin Receptor-Positive Post-Streptococcal Acute Glomerulonephritis Showing Full-House Pattern: A Case Report.","authors":"Yusuke Takahashi, Naoto Kawata, Hiroki Nishiwaki, Yoshinori Sato, Toshiharu Ueno, Takashi Oda, Fumihiko Koiwa","doi":"10.1159/000546484","DOIUrl":"10.1159/000546484","url":null,"abstract":"<p><strong>Introduction: </strong>Post-streptococcal acute glomerulonephritis (PSAGN) is a disease in which patients develop hematuria and leg edema following streptococcal infection, which may lead to acute nephritic syndrome and nephrotic syndrome. We present a case involving acute kidney injury and nephrotic syndrome with nonspecific pathological findings for PSAGN, which posed diagnostic challenges.</p><p><strong>Case presentation: </strong>A 25-year-old man presented with leg edema, cough, nephrotic syndrome, severe kidney dysfunction, and hematuria. Blood tests showed elevated antistreptolysin O levels and decreased complement C3 levels; therefore, PSAGN was suspected. Light microscopy revealed membranoproliferative glomerulonephritis, immunofluorescence staining revealed a full-house pattern, and electron microscopy revealed subendothelial deposition. The diagnosis was difficult, however, positive glomerular staining for nephritis-associated plasmin receptor and plasmin activity strongly suggested an infection-related etiology of glomerulonephritis. Treatment included the administration of 500 mg of methylprednisolone for 3 days, followed by 4 weeks of treatment with 50 mg of prednisolone. Subsequently, the dosage was reduced to 40 mg, and the patient was discharged. Urinary findings revealed resolution of hematuria 1 year after discharge.</p><p><strong>Conclusion: </strong>When PSAGN is suspected and other diseases are difficult to exclude, nephritis-associated plasmin receptor staining should be considered.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"198-205"},"PeriodicalIF":0.9,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249919","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":"The Diagnostic Challenge of Potassium-Wasting and Hypertension in Pregnancy: Lessons from a Geller Syndrome Workup.","authors":"Justin David Tse, Ryan Lin, Jackson Wang","doi":"10.1159/000547158","DOIUrl":"10.1159/000547158","url":null,"abstract":"<p><strong>Introduction: </strong>Hypokalemia in pregnancy is usually attributed to benign causes, yet persistent hypokalemia with hypertension raises concerns for rare renal potassium-wasting disorders. Among these, Geller syndrome, a rare mineralocorticoid receptor mutation that can be activated by progesterone, can precipitate severe hypokalemia and hypertension unique to pregnancy due to heightened receptor sensitivity. This case underscores the need to recognize and systematically evaluate potassium-wasting syndromes in pregnancy to optimize outcomes and inform clinical decision-making.</p><p><strong>Case presentation: </strong>We present a 33-year-old woman, G6P2, at 21w6d of gestation, presented with abdominal pain, marked hypokalemia (2.6 mEq/L), and systolic blood pressures in the 150s. She reported no previous history of hypertension or diuretic use and had no significant family history. Initial assessment excluded common etiologies, such as preeclampsia, prompting an expanded renal workup. Laboratory findings revealed profound renal potassium-wasting, evidenced by a trans-tubular potassium gradient of 11 and a urine potassium-to-creatinine ratio of 45, alongside low aldosterone levels, normal cortisol, and thyroid function. She experienced persistent hypokalemia despite aggressive repletion which led to suspicion of Geller syndrome. Continued potassium supplementation, dietary guidance, and fetal delivery eventually led to stable potassium levels.</p><p><strong>Conclusion: </strong>This case highlights the diagnostic complexities of addressing refractory hypokalemia and hypertension in pregnancy, advocating for the consideration of rare etiologies like Geller syndrome. Although negative in this instance, the suspicion of Geller syndrome informed a meticulous diagnostic approach, underscoring the importance of a comprehensive evaluation and genetic counseling in similar presentations. Such awareness can enhance clinicians' diagnostic frameworks, equipping them to identify and manage rare syndromes if needed. By expanding the differential diagnosis for persistent hypokalemia and hypertension in pregnancy, this case underscores the potential for improved maternal-fetal outcomes through informed and targeted management strategies.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"177-182"},"PeriodicalIF":0.9,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249902","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":"Acute Interstitial Nephritis Associated to Pertussis Infection: A Case Report and Review of the Literature.","authors":"Gabriel Sartori Pacini, Renata Asnis Schuchmann, Luis Henrique Vizioli, Lucas Gobetti da Luz, Illan George Balestrin, Karla Lais Pêgas, Milton Kalil, Maurício Lutzky","doi":"10.1159/000547404","DOIUrl":"10.1159/000547404","url":null,"abstract":"<p><strong>Introduction: </strong>Whooping cough (pertussis) is an acute respiratory infection primarily caused by <i>Bordetella pertussis</i>, which predominantly affects children. While the disease commonly presents with upper respiratory symptoms, it can lead to severe complications such as pneumonia, encephalopathy, and even death. The association between respiratory infections and renal injury, specifically acute interstitial nephritis (AIN), remains poorly understood. This report describes a rare case of AIN in a patient with whooping cough.</p><p><strong>Case presentations: </strong>A 73-year-old male with a history of systemic arterial hypertension, dyslipidemia, and previous left nephrectomy presented with a 5-day history of fatigue, fever, cough, and nasal obstruction. Initial laboratory findings revealed mild leukocytosis and significantly elevated serum creatinine (5.17 mg/dL), with urinalysis showing leukocyturia and proteinuria. A respiratory infection panel confirmed <i>B. pertussis</i>, and the patient was treated with azithromycin. Despite improvement in respiratory symptoms, renal function remained impaired. Renal biopsy revealed moderate tubulointerstitial nephritis, and the patient was treated with prednisone, leading to gradual recovery of renal function, with serum creatinine decreasing to 2.3 mg/dL at discharge and 1.85 mg/dL 3 weeks later.</p><p><strong>Conclusion: </strong>This case highlights the potential renal complications of whooping cough, specifically AIN, a rarely reported association. Although respiratory infections such as pertussis are well known for pulmonary involvement, clinicians should be aware of the possibility of concurrent renal injury. Prompt recognition and appropriate treatment, including corticosteroids in the case of AIN, can lead to significant improvement in renal function. Further research is needed to better understand the mechanisms by which <i>B. pertussis</i> may cause renal damage.</p>","PeriodicalId":9599,"journal":{"name":"Case Reports in Nephrology and Dialysis","volume":"15 1","pages":"183-188"},"PeriodicalIF":0.9,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145249970","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}