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Renal limited sarcoidosis is an exceptionally rare condition characterized by non-caseating granulomas confined solely to the kidneys, without involvement of other organs. Its diagnosis is challenging because of the absence of systemic manifestations. We present a case of a 74-year-old woman with a history of type 2 diabetes mellitus, papillary thyroid carcinoma, and osteoporosis, who showed progressive renal dysfunction. Laboratory findings revealed elevated serum creatinine and urinary ß2-microglobulin, indicating tubular injury. Kidney biopsy demonstrated granulomatous interstitial nephritis with non-caseating epithelioid cell granulomas. Other potential causes, including infections, drug-induced nephritis, and autoimmune diseases were excluded. Chest computed tomography and gallium-67 scintigraphy revealed no extrarenal involvement. Based on these findings, we diagnosed the patient as having renal limited sarcoidosis. The patient was treated with low dose of oral prednisolone, resulting in significant improvement in renal function and normalization of laboratory parameters. The present case underscores the importance of considering the possibility of renal limited sarcoidosis on differentiating the case with unexplained renal dysfunction, especially when non-caseating granulomas are identified on kidney biopsy and other causes have been excluded. Corticosteroids remain the cornerstone of treatment, with most patients responding favorably. However, in steroid-resistant cases, alternative immunosuppressive agents such as mycophenolate mofetil and infliximab have been employed, though their efficacy and safety require further investigation. In this article, we present this rare case in addition to providing comprehensive literature review of previously cases to summarize clinicopathological characters, treatment strategies, and renal outcomes of renal-limited sarcoidosis for future clinical management.

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BACKGROUND: Kidney involvement in pediatric sarcoidosis is rare and often underrecognized, leading to diagnostic delays and treatment challenges. We report six patients with renal sarcoidosis to highlight their diverse presentations and outcomes and challenges in management. METHODS: Medical records of patients diagnosed with renal sarcoidosis during 2020-24 were reviewed. Sarcoidosis was diagnosed based on clinical and histological features and exclusion of alternative causes and managed according to unit protocols. Information on clinical features, laboratory and radiologic findings, histopathology, treatment, and follow-up were compiled. RESULTS: We present six patients with sarcoidosis, presenting with kidney involvement at the age of 1.5-14 years, and followed up for 7-138 months. All patients had acute kidney injury (AKI) of whom two required hemodialysis. Proteinuria was present in all patients, while four patients had microscopic hematuria or leukocyturia. Hypercalcemia with hypercalciuria, distal renal tubular acidosis, and nephrocalcinosis were seen in five, two, and one case, respectively. Granulomatous interstitial nephritis was confirmed histologically in all cases. While initial therapy with corticosteroids led to clinical remission in all cases, five patients had nine relapses, necessitating second-line immunosuppression with mycophenolate mofetil, azathioprine, or methotrexate; one patient received antitumor necrosis factor therapy. Median eGFR at last follow up was 59.7 (range 12.7-132) ml/min/1.73 m2; three progressed to chronic kidney disease (CKD) stages G3-G5. CONCLUSIONS: Kidney involvement in pediatric sarcoidosis manifests in diverse forms, ranging from isolated biochemical abnormalities to severe AKI. While prompt immunosuppression might preserve kidney function, patients require close monitoring for relapses, and progression to CKD.

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A male in his 50s presented to the renal department with a diagnostic challenge of an unexplained kidney injury. Antiphospholipid antibody syndrome and oral anticoagulation augmented the risk for a renal biopsy. This, along with relatively static estimates of glomerular filtration rate combined to delay renal biopsy and definitive renal diagnosis by 6 months. The late emergence of symptomatic bilateral anterior uveitis consolidated the diagnosis of tubulointerstitial nephritis and uveitis (TINU) syndrome but it also highlighted a lack of systemic early screening for ocular disease in the renal clinic. When faced with a diagnostic challenge, clinicians are more likely to find clinical conditions they are actually looking for. Increased awareness of TINU, earlier screening for ocular symptoms at presentation and/or examination for asymptomatic uveitis when a diagnosis of tubulointerstitial nephritis is being considered is recommended. Furthermore, early screening in cases of bilateral anterior uveitis for existing kidney issues should be pursued.

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This report describes a man in his late 50s who underwent donation-after-circulatory-death kidney transplantation in 2012, due to end-stage kidney disease of unknown origin. More than a decade post-transplant, he presented with a progressive decline in graft function after maintenance immunosuppression had been reduced due to multiple skin carcinomas and the prolonged time since transplantation. Kidney biopsy revealed chronic-active tubulointerstitial nephritis with positive immunohistochemical staining for SV40, initially raising suspicion for BK polyomavirus-associated nephropathy. However, quantitative PCR (qPCR) analysis for BKPyV in both plasma and tissue was negative. In contrast, qPCR for JC polyomavirus (JCPyV) was positive in both plasma and biopsy tissue, leading to the diagnosis of JC polyomavirus nephropathy. Despite the reduction of immunosuppressive therapy, the patient experienced ongoing deterioration of graft function. Our report adds to the limited but growing body of literature on JCPyV and emphasises the need for increased clinical awareness and further research into its prevalence, pathogenesis and optimal management in kidney transplant recipients.

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Tubulointerstitial nephritis (TIN) is a frequent cause of acute kidney injury. TIN has a reported incidence ranging from 1% to 10% of all renal biopsies. Among patients with chronic renal failure, the incidence ranges from about 22% to 33.5%. We studied the histological features of renal biopsies with TIN, evaluated its etiology and correlated TIN with clinical features and investigations. Our study extended over a period of seven years, with 50 cases. The slides were stained with hematoxylin and eosin and special stains like periodic acid-Schiff, Jones methenamine silver and Masson's trichrome. All adequate renal biopsies showing features of acute and chronic TIN were included in our study. Renal biopsies showing features of only primary glomerular pathology and inadequate biopsies were excluded from the study. TIN accounted for 14.84% of all the renal biopsies received in our histopathology section within this period, with 74% cases presenting as acute renal failure. The mean age of our study group was 39 years, with the male-female ratio being 1:1.63. Drug-induced TIN accounted for 42% of the cases, making it the most common cause; 48% of the cases of drug-induced TIN were attributed to the use of nonsteroidal anti-inflammatory drugs. The other causes were immunological, infectious, metabolic, vascular, plasma cell dyscrasias, T-cell mediated and idiopathic. TIN is an important cause of acute renal failure, with drug-induced TIN constituting almost half the cases. These cases can be reversed if caught early, making renal biopsy a valuable modality in diagnosing TIN in cases of acute renal failure.

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Granulomatous interstitial nephritis (GIN) is rare in childhood and is associated with poor outcomes. We report a 6-year-old girl who developed nephrotic-range proteinuria following chronic non-steroidal anti-inflammatory drug (NSAID) use for juvenile idiopathic arthritis (JIA). Other possible etiologies were ruled out, and the diagnosis of GIN was confirmed by renal biopsy. NSAIDs were henceforth withheld and prednisolone was started, which resulted in amelioration of proteinuria. Strong suspicion, quick diagnosis and early initiation of therapy improve the outcome in GIN and prevents or delays kidney failure.

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A 55-year-old man presented to the emergency department (ED) with diffuse abdominal pain, vomiting, and anuria following a night of heavy alcohol intake. The patient's medical history included hypertension. Two weeks prior to presentation, he was prescribed etoricoxib for back pain. On presentation, he was found to have severe acute kidney injury, and dialysis was initiated. Renal biopsy showed acute interstitial nephritis with numerous eosinophilic infiltrates. Despite stopping etoricoxib and initiating high-dose steroids, kidney function did not improve. The administration of benralizumab-an anti-CD125 antibody-resulted in rapid and complete recovery of kidney function. This case report highlights the potential role of benralizumab in the treatment of drug-induced interstitial nephritis with eosinophiluria.

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Background: Patients affected by very early onset inflammatory bowel disease (VEO-IBD) are frequently refractory to standard treatments. Despite the lack of randomized clinical trials, vedolizumab emerged as an effective and safe alternative treatment in VEO-IBD resistant to TNF antagonists. Here, we present a case of VEO-IBD with ulcerative colitis (UC) phenotype developing renal injury after vedolizumab administration. Case presentation: An 11-year-old female patient with VEO-UC was referred to our clinic for fever, nausea, and fatigue. She was treated with vedolizumab for 1 year due to steroid-dependent disease and failure of multiple therapies, including anti-TNF agents. At admission, she was in steroid-free clinical and endoscopic remission, with leukocytosis, increased inflammatory markers, and a rise in serum creatinine. Urine samples revealed persistent leukocyturia over the past 8-10 months with the absence of lower urinary tract symptoms and negative serial urine culture. MRI showed swollen-looking kidneys with bilateral irregular Diffusion-Weighted Imaging (DWI) signal restriction. Kidney biopsy revealed the presence of acute tubular damage with a mixed interstitial inflammatory infiltrate consistent with drug-induced acute tubulointerstitial nephritis (TIN). After prompt start of systemic glucocorticoid therapy and temporary discontinuation of vedolizumab, normalization of renal function and urinalysis was observed. Vedolizumab was restarted after 2 months, pre-medicated with steroids. The follow-up renal biopsy performed after 6 months showed a regression of the histological pattern, with chronic signs characterized by mild tubular atrophy and interstitial fibrosis. Conclusion: Vedolizumab-related acute TIN is a potentially severe complication, rarely described in adult patients. We report the first case of VEO-IBD with a probable vedolizumab-related acute TIN treated with corticosteroids, with a good response and maintenance of vedolizumab. Persisting sterile leukocyturia could represent an early sign.

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BACKGROUND Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have become important in the treatment of diabetic kidney disease (DKD). Despite their reno-protective effect, kidney injury from GLP-1 RAs has been rarely reported. The reported kidney injuries varied from mild symptoms to dialysis at presentation and occurred 2 days to 2 years after drug initiation. We report a case of a patient with DKD who developed an episode of interstitial nephritis after dulaglutide administration. CASE REPORT A 63-year-old woman with stage 3b diabetic kidney disease and depressive disorder was prescribed dulaglutide 0.75 mg/week subcutaneously in August 2023 due to persistent albuminuria despite receiving the maximum tolerated dose of azilsartan. Sodium-glucose cotransporter-2 inhibitor was not prescribed in this case due to her frequent urinary tract infections. Serum creatinine at 2-month follow-up increased and then doubled despite reduction in the azilsartan dose. Potentially nephrotoxic medications were discontinued and no other possible causes of kidney injury, including volume depletion, were presented. Kidney biopsy revealed active interstitial nephritis and diabetic nephropathy without accumulation of immune complex. After discontinuing dulaglutide, there was an almost complete recovery of kidney function without steroid therapy. Azilsartan and chlorthalidone could then be successfully rechallenged. CONCLUSIONS Despite the established renoprotective effect of GLP-1 RAs, acute-to-chronic tubulointerstitial nephritis occasionally occurs, requiring vigilant monitoring after drug initiation or titration. Nevertheless, this does not prevent the prescription of GLP-1 RAs to alleviate DKD progression in certain patients. Treatment includes drug discontinuation and steroid therapy in non-responders.

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RATIONALE: Tubulointerstitial nephritis uveitis syndrome (TINU) is a rare form of acute interstitial nephritis accompanied by uveitis. However, few cases of TINU associated with Fanconi syndrome (FS) have been reported, and the clinical characteristics and optimal management of this rare association remain poorly defined. PATIENT CONCERNS: In this case report, we aimed to describe 2 cases of TINU associated with FS and their management, emphasizing the importance of recognizing FS as a potential complication in patients with TINU. DIAGNOSES: Two adult patients with TINU and FS were evaluated. Both presented with renal insufficiency, hypouricemia, hypophosphatemia, hypokalemia, renal glycosuria, low-molecular-weight proteinuria, and uveitis. One patient also had renal tubular acidosis. Renal biopsy revealed acute interstitial nephritis in both cases, with one case additionally showing immunoglobulin A nephropathy. INTERVENTIONS/OUTCOMES: Systemic and ocular topical corticosteroids were administered, and potassium citrate was used to correct renal tubular acidosis. Renal function, electrolyte levels, and urinalysis results normalized in both patients. LESSONS: In patients with TINU and renal tubular dysfunction (such as low-molecular-weight proteinuria, hypophosphatemia, and hypouricemia) the possibility of secondary FS should be considered. Along with corticosteroid therapy, timely treatment of renal tubular acidosis is essential.

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Biopsy-confirmed anticancer drug-induced kidney injury is underreported. This study aimed to characterize its clinicopathological features and outcomes. We retrospectively analyzed 52 patients with biopsy-proven anticancer drug-induced nephrotoxicity (2005-2024). Patients were classified into chemotherapy drugs (CTD, n = 25), molecularly targeted therapies (MTT, n = 22), and immune checkpoint inhibitors (ICI, n = 5; PD-1 inhibitors). The CTD group (e.g. cisplatin, capecitabine, gemcitabine) caused frequent acute kidney injury (AKI, 80%), with acute tubulointerstitial nephritis (ATIN, 32%). Notable glomerular lesions in the CTD group included thrombotic microangiopathy (TMA, 12%), minimal change disease (8%), and focal segmental glomerulosclerosis (8%). The MTT group (e.g. bevacizumab, lenvatinib, sorafenib) had higher proteinuria (0.4 vs. 3.1 vs. 0.7 g/24h; p < 0.05) and TMA incidence (86%). MTT-induced TMA produced distinct subtypes: anti-VEGF(R) therapy (n = 11) caused glomerular capillary ballooning (100%); non-VEGFR-TKIs (n = 4) were associated with segmental glomerulopathy; combined anti-VEGF/VEGFR-TKI (n = 4) resulted in more extensive and severe TMA (>75% of glomeruli). ICI therapy (nivolumab, camrelizumab, sintilimab) led to early AKI, mainly ATIN (80%), with glomerular IgA deposition (80%) and low serum C3 (60%). After a median follow-up of 23.0 months, MTT showed faster AKI recovery than CTD (0.5 vs. 8.0 months; p = 0.002). Anticancer drugs induce distinct nephrotoxic patterns. CTD causes direct cytotoxicity and high irreversible injury risk. MTT drives functional TMA, and new-onset hypertension with proteinuria should raise concern for anti-VEGF-related TMA. ICI triggers immune dysregulation with humoral disturbances, and AKI with low serum C3 can be a safety signal for clinical monitoring.

Anticancer drugs induce distinct nephrotoxic patterns: chemotherapy drugs (CTD) are associated with direct cellular toxicity and a high risk of irreversible kidney injury; molecularly targeted therapies (MTT) drive functional thrombotic microangiopathy; immune checkpoint inhibitors (ICI) may trigger immune dysregulation.Biopsy Guides Management: Renal biopsy is essential for accurate diagnosis, especially in MTT-related injury, where pathological heterogeneity correlates with drug targets and affects treatment approaches.Prognostic Heterogeneity: Injury from MTT usually resolves quickly after drug discontinuation, while CTD-related injury carries a higher risk of irreversible damage. ICI-related injury typically responds to steroids but may have a poorer outcome if glomerular pathology is present.Novel Immune Mechanisms: ICI-associated injury frequently involves glomerular IgA deposition and complement activation, suggesting that humoral immunity may play a role beyond classic T-cell-mediated inflammation.Framework for Onconephrology: This large biopsy-based study helps clinicians optimize management across three anticancer drug classes.

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We report the case of a 79‒year‒old woman diagnosed with drug‒induced tubulointerstitial nephritis during treatment with capivasertib. The patient received fulvestrant and capivasertib, and on day 11 of therapy, she was admitted to the hospital with appetite loss, rash, and hyperglycemia. Continuous insulin therapy was initiated. The following day, she developed renal dysfunction. Given elevated levels of urinary protein and serum ß2‒microglobulin, a diagnosis of capivasertib‒induced tubulointerstitial nephritis was made. Steroid pulse therapy was administered after initial management of renal dysfunction. Proteinuria improved with treatment. Although capivasertib‒the first AKT inhibitor approved in Japan‒is associated with several adverse effects including hyperglycemia, rash, and diarrhea, tubulointerstitial nephritis has not previously been reported in Japan.

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The increase use of vaping, especially in the younger population, has led to increased scrutiny of its health effects, particularly on renal function. This article reviews the current literature on the association between vaping, nicotine exposure, and renal impairment, focusing on the development of acute kidney injury (AKI) and chronic kidney disease (CKD). Nicotine and other chemicals in e-liquids may induce microangiopathy, leading to vasoconstriction and reduced renal perfusion, thus contributing to AKI. Chronic exposure to nicotine also promotes an inflammatory response, increasing the risk of interstitial nephritis. Additionally, glomerular damage due to continuous use of vapers has been linked to albuminuria and progression of focal segmental glomerulosclerosis (FSGS), a condition that can lead to CKD. This article highlights the need for further research to clarify the kidney risks associated with vaping and provides information for public health policies on nicotine use.

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We report a unique case of membranous nephropathy and tubulointerstitial nephritis preceding neurological manifestations of Bing-Neel syndrome, a rare variant of Waldenström macroglobulinemia. A 46-year-old man presented with nephrotic syndrome, and kidney biopsy revealed membranous nephropathy with phospholipase A2 receptor positivity and IgG4 predominance. Despite initial partial remission with corticosteroids and cyclosporine, neurological symptoms emerged alongside nephrotic syndrome relapse two years after onset. Diagnostic workup revealed serum monoclonal IgM kappa, abnormal lymphoplasmacytic cells in bone marrow and cerebrospinal fluid, and MYD88 L265P mutation in the latter, confirming Bing-Neel syndrome. Immunostaining of the initial kidney biopsy demonstrated IgM-kappa-positive lymphoplasmacytic infiltration consistent with the monoclonal protein. After bendamustine-rituximab therapy showed partial effectiveness, tirabrutinib, a Bruton tyrosine kinase inhibitor, achieved complete remission of both renal and neurological manifestations with sustained response over three years. Immunofluorescence staining revealed increased nuclear factor (NF)-κB and STAT3 expression in infiltrating immune cells and elevated NF-κB in surrounding tubular epithelial cells, suggesting activation of these pathways downstream of the MYD88 mutation in kidney pathology. Our findings suggest a potential contribution of Bruton's tyrosine kinase signaling to both kidney and neurological pathology in Bing-Neel syndrome, with tirabrutinib achieving clinical improvement in both organ manifestations.

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Studies examining IgG subclasses within circulating immune complexes (CICs) in patients with IgG4-related disease remain scarce. A Japanese man in his 50s with a history of diabetes mellitus and chronic pancreatitis was referred to our department because of an increase in serum creatinine levels. Serum IgG and IgG4 levels were markedly high, accompanied by eosinophilia and elevated serum IgE levels. C3 hypocomplementemia and an increase in CICs were also noted, and imaging revealed swollen mediastinal lymph nodes. Renal biopsy revealed extensive tubulointerstitial nephritis with numerous IgG4-positive plasma cells and dense interstitial fibrosis. The patient was diagnosed with IgG4-related disease, and glucocorticoid therapy was initiated; renal function, serological abnormalities, and swelling of the mediastinal lymph nodes improved. Subsequent analyses revealed that the patient's CICs mainly comprised IgG4 and that there was tubular deposition of complement components C1q, C4d, C3, and C5b-9 in the renal biopsy tissue, suggesting that immune complexes containing IgG4 activated the complement pathway in circulation and locally in the kidneys. Hypocomplementemia and CICs are observed in a subset of patients with IgG4-related diseases; however, the underlying mechanisms remain unclear. Further accumulation of IgG4-related disease cases is required to evaluate the possibility of IgG4-mediated complement activation.

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BACKGROUND: Systemic lupus erythematosus (SLE) is a chronic inflammatory disease that affects multiple organ systems, and lupus nephritis (LN) primarily involves glomerular, vascular and tubulointerstitial lesions. Renal tubulointerstitial lesions are almost always present alongside glomerular lesions, with isolated renal tubulointerstitial LN being very rare. The aim of this study was to evaluate the clinicopathological features, differential diagnosis, treatment and prognosis of predominant tubulointerstitial lupus nephritis (PTILN). CASE PRESENTATION: We present the case of a 64-year-old Chinese male with severe SLE. The diagnosis of SLE was confirmed on the basis of proteinuria, positive antinuclear antibodies, and immunological and haematological disorders. Renal biopsy revealed severe chronic tubulointerstitial nephritis with excessive immune complex deposition in the tubular basement membrane (TBM), mild glomerular lesions and minimal immune complex deposition, suggesting predominant tubulointerstitial LN. The patient was treated with steroids and mycophenolate mofetil, leading to stabilization of renal function. In the literature review, we identified a total of 18 patients whose predominant tubulointerstitial LN was reported. In our analysis, we evaluated the clinical and pathological features, treatment, and prognosis of this condition in these patients. CONCLUSIONS: This case series reinforces PTILN as a distinct LN variant characterized by dominant tubulointerstitial inflammation and TBM immune deposits. Although PTILN shares clinical features with classic LN, PTILN exhibits notable heterogeneity in demographics, pathology, and outcomes, and its pathogenesis, diagnostic criteria, and optimal management require further elucidation.

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Tubulointerstitial kidney disease can be recognized histologically as tubulointerstitial injury that is out of proportion to glomerular or vascular pathology. While recognizable as a histologic entity, determining a more precise underlying etiology for tubulointerstitial disease can be a diagnostic challenge. This review presents a clinicopathologic approach intended to help nephrologists and pathologists narrow the clinical differential diagnosis of tubulointerstitial disease. Inflammatory tubulointerstitial disease can often be subcategorized based on the presence of specific types of inflammatory infiltrates, such as eosinophils, neutrophils or granulomas. Recognition of these inflammatory phenotypes raises and lowers some entities in the differential diagnosis. Broadly speaking, underlying causes of inflammatory tubulointerstitial disease include drug reaction, infection, and autoimmune diseases. The most common causes of acute noninflammatory tubulointerstitial disease are ischemic and toxic tubular injuries. Much of the time there is substantial overlap in the morphology of ischemic and toxic tubular injury, but there are distinctive findings in noninflammatory tubulointerstitial disease, including casts and crystals, that may allow for a more specific histologic diagnosis that maps to a narrower clinical differential diagnosis. Ultimately, understanding the root cause of tubulointerstitial disease requires careful integration of clinical history with histopathologic findings.

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Chronic kidney disease of undetermined cause is characterized by distinctive histopathological features predominantly affecting the tubulointerstitial compartment of the kidney. Kidney biopsies from affected individuals consistently demonstrate interstitial fibrosis and tubular atrophy as the hallmark findings, observed in over 80-90% of cases, with severity correlating closely with decreased glomerular filtration rate. Interstitial inflammation is generally mild or absent in early disease stages but may increase in advanced fibrosis, with T lymphocytes and macrophages predominating. Tubulitis and acute tubular injury are rare and usually restricted to patients presenting acutely. Electron microscopy reveals ultrastructural tubular changes such as cell detachment, basement membrane thickening, and collagen fibril deposition, though these are nonspecific. Glomerular abnormalities are typically secondary, including glomerulosclerosis in less than 50% of glomeruli, glomerulomegaly, and periglomerular fibrosis, reflecting compensatory hypertrophy or reduced nephron number. Immune complex deposition is minimal or absent. Vascular changes are generally not prominent. Despite the diagnostic value of kidney biopsy in chronic kidney disease of undetermined cause, clinical use is limited by socioeconomic factors, procedural risks, and lack of targeted therapies. Standardized biopsy protocols and reporting are essential for improving diagnosis, prognosis, and understanding disease mechanisms to guide future research and treatment strategies.

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Tubulointerstitial nephritis (TIN) is a rare heterogenous kidney disease and outcomes depend upon many factors including patient characteristics, clinical presentation and histopathological features on kidney biopsy. When considering short-term kidney outcomes, about 20% of adult patients with acute TIN will require dialysis, although many will fully or partially recover without need for maintenance kidney replacement therapy. However, current evidence suggests that long-term kidney outcomes of patients with TIN are far less favorable than originally thought. Risk factors for adverse kidney outcomes include patient characteristics (e.g., older age, hypertension), a higher degree of proteinuria, recurrent acute TIN episodes and signs of disease chronicity or granulomatous interstitial nephritis on kidney biopsy. Pediatric patients have a better long-term prognosis, although a significant proportion of patients will develop CKD as well. In general, drug-induced acute TIN has a better prognosis when compared with autoimmune etiologies, particularly if the inciting drug is discontinued early in the disease course and re-exposure is avoided. Autoimmune etiologies frequently cause CKD, partially because they are associated with recurrent acute TIN episodes. In this review, we summarize the available data regarding prognosis and outcomes of acute and chronic TIN for various etiologies of TIN.

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Acute tubulointerstitial nephritis (ATIN) is one of the leading causes of acute kidney injury (AKI), accounting for approximately 15-27% of biopsy-proven cases of AKI. While some patients recover kidney function with timely intervention, a subset of patients may progress to chronic kidney disease and around one-third of the patients will require chronic dialysis. Drug-induced ATIN is the most common form and is often associated with nonsteroidal anti-inflammatory drugs, antibiotics, and proton pump inhibitors. Infections, autoimmune disorders, such as Sjögren's syndrome and sarcoidosis contribute to a smaller proportion of cases. Clinically, ATIN presents with a wide spectrum of symptoms ranging from asymptomatic AKI to systemic manifestations such as fever, rash, arthralgia, and eosinophilia. Urinalysis often reveals sterile pyuria, hematuria, and occasionally, white blood cell casts. Proteinuria is typically mild (<1.5 g/24 hours. Definitive diagnosis requires kidney biopsy, which reveals the presence of an extensive interstitial infiltrate, mainly composed of lymphocytes and monocytes, along with interstitial edema, and varying degrees of tubular injury. Early identification and management are critical to prevent irreversible kidney damage. So far, the optimal treatment of this entity is not yet well characterized but treatment strategies for ATIN must focus on prompt discontinuing the offending agent, supportive care, and corticosteroid therapy.