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BACKGROUND: Intravesical bacillus Calmette-Guerin (IVBCG) is considered the most optimal follow-up therapy for high-risk urothelial cancers. Although side effects such as cystitis, hematuria, and low-grade fever are common, they are generally mild. Severe reactions involving the kidneys are extremely rare. Here, we present the case of a 64-year-old male who developed acute renal failure due to acute tubulointerstitial nephritis (ATIN) following the first IVBCG administration. We have also conducted a literature review concerning IVBCG-induced nephritis. CASE REPORT: A 64-year-old male presented to the Nephrology Department with acute kidney injury indicators and hematuria. The patient was suffering from high-grade papillary urothelial carcinoma. Transurethral resection of the bladder tumor was performed twice and followed by one IVBCG administration - two days before the symptoms occurred. The latest follow-up cystoscopy excluded the recurrence of the cancer. Laboratory tests displayed hyperkalemia, decreased glomerular filtration rate (GFR = 4 ml/min/1.73 m2), elevated C-reactive protein, and acute metabolic acidosis. Urinalysis showed proteinuria (900 mg/24 h), leukocyturia, and erythrocyturia (20,402.7 per microliter). Renal ultrasound demonstrated slight bilateral renal enlargement. The patient was identified with acute tubulointerstitial nephritis (ATIN). The treatment involved intravenous methylprednisolone (250 mg three times every two days and then 125 mg four times every two days), followed by oral methylprednisolone (24 mg and 12 mg daily alternately for a week). Piperacillin and tazobactam, probiotics, and proton pump inhibitors were also administered. Hemodialysis was conducted three times. Two weeks after the admission, a significant improvement was observed: creatinine decreased to 2.04 mg/dl, and GFR increased to 33 ml/min/1.73 m2. The patient was discharged with a recommendation to reduce the dose of glucocorticosteroids and continued in the outpatient clinic. CONCLUSIONS: IVBCG may lead to acute kidney injury due to ATIN. Symptoms may occur as early as after the first IVBCG, contrary to previous reports. Patients should be regularly assessed for potential complications, including creatine level measurement, after each IVBCG treatment. [ABSTRACT FROM AUTHOR]

Introduction: Acute promyelocytic leukemia (APL), classified as Subtype M3 of acute myeloid leukemia, is known for its relatively favorable prognosis, primarily due to the high effectiveness of all-trans retinoic acid (ATRA) in treating the maturation block. However, it is essential to be aware of potential complications such as ATRA syndrome, which can affect 5%–25% of patients and manifest with symptoms such as fever, interstitial pulmonary infiltration, pleural/pericardial effusion, and acute renal failure. Methods: We present the case of a 47-year-old female with a history of hypertension, who experienced rash, fever, and reduced urine output during the induction phase with ATRA. Her serum creatinine levels exhibited a rapid increase from 2.63 mg/dL on October 07, 2022, to 7 mg/dL on October 18, 2022, despite having normal-sized kidneys and normal corticomedullary differentiation. A renal biopsy conducted on October 20, 2022, revealed features consistent with active tubulointerstitial nephritis, with direct immunofluorescence showing no significant glomerular immune deposits. A total of 17 hemodialysis sessions were performed. Results: A subsequent bone marrow examination conducted on October 26, 2022, demonstrated a hypercellular aspirate with normal morphology. However, due to the persistence of renal failure, a repeat biopsy was performed, revealing severe acute tubular injury. Pulse steroids were initiated, and ATRA was discontinued, resulting in an improvement in renal function. Conclusion: This case highlights an instance of acute, early, and severe differentiation syndrome (DS) occurring after induction therapy in a patient with APL. The DS in this case was particularly severe, leading to renal failure necessitating hemodialysis. The prompt initiation of pulse steroids and discontinuation of ATRA proved to be effective in managing this complication. Clinicians should remain vigilant for DS and its potential complications, including acute kidney injury and acute tubulointerstitial nephritis, when treating patients with APL. [ABSTRACT FROM AUTHOR]

Background and objectives In clinical practice, some patients are diagnosed with diabetic nephropathy (DN) combined with acute tubulointerstitial nephritis (ATIN) through renal biopsy. There is relatively little research on the treatment and prognosis of such patients, and no consensus exists on the use of glucocorticoid for treatment. Therefore, our study explores the progression of DN combined with ATIN and the renal outcomes after treatment with glucocorticoid.Methods This study retrospectively analyzed patients diagnosed with DN combined with ATIN through renal biopsy at our center from January 1, 2015, to December 31, 2021. We collected general patient information, laboratory indicators, renal pathology indicators, and the glucocorticoid usage after kidney biopsy. Follow-up data were collected from medical records. Statistical analysis methods included t-tests, non-parametric tests, and chi-square tests. Univariate and multivariate Cox regression analyses were used to evaluate the risk factors for renal endpoint events in patients. Statistical significance was defined as p-values < 0.05.Results In this study, a total of 67 patients were included. The subjects were divided into two groups based on whether they received glucocorticoid treatment: 33 patients in the steroid group and 34 in the non-steroid group. In the steroid group, 19 patients reached the renal endpoint event, which was significantly higher than in the non-steroid group (57.58% vs. 29.41%, p = 0.038). Univariate Cox regression analysis showed that serum creatinine (HR = 1.008, p

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Acute porphyria is a group of metabolic disorders characterized by a deficiency in enzymes involved in heme biosynthesis. A 21-year-old female with abdominal pain and an altered sensorium, eventually leading to a diagnosis of acute porphyria. Glucose treatment and supportive measures improved her general condition. Renal biopsy showed persistent renal dysfunction, which revealed acute tubulointerstitial nephritis with 5-10% interstitial fibrosis and tubular atrophy. This highlights a unique manifestation of acute porphyria involving the kidney and emphasizes the importance of considering acute tubulointerstitial nephritis as a cause of renal dysfunction in acute porphyria.

Introduction: Acute tubulointerstitial nephritis (ATIN) is a well-recognized cause of acute kidney injury (AKI) due to the tubulointerstitial inflammation. The aim of this study was to explore the clinical features, outcomes, and responses to corticosteroid treatment in patients with ATIN. Methods: Patients with biopsy-proven ATIN, who were diagnosed between 1994 and 2016 at the Department of Nephrology, Charles University, First Faculty of Medicine, and General University Hospital in Prague, were included in the study. Patient demographics, the aetiological and clinical features, the treatment given, and the outcome at 1 year of follow-up were extracted from patient records. Results: A total of 103 ATIN patients were analysed, of which 68 had been treated with corticosteroids. There was no significant difference in the median serum creatinine 280 (169–569) µmol/L in the conservatively managed group versus 374 (249–558) µmol/L in the corticosteroid-treated group, p = 0.18, and dependence on dialysis treatment at baseline at the time of biopsy (10.3 vs. 8.6%). During the 1 year of follow-up, those ATIN patients who had been treated with corticosteroids did better and showed greater improvement in kidney function, determined as serum creatinine difference from baseline and from 1 month over 1-year period (p = 0.001). Conclusions: This single-centre retrospective cohort study supports the beneficial role of the administration of corticosteroid therapy in the management of ATIN. [ABSTRACT FROM AUTHOR]

Introduction: Acute kidney injury (AKI) in cancer patients receiving immune checkpoint inhibitors (ICIs) may recognize multiple causes. Here, we reviewed cases of biopsy-proven acute tubulointerstitial nephritis (ATIN) to describe the clinical characteristics and outcomes of this condition. Method: We conducted a pooled analysis of clinical cases of ICI-related biopsyproven ATIN up to 1 May 2022. We collected data on clinical characteristics, AKI, biopsy findings, laboratory examinations, and renal outcomes. Results: Eighty-five patients (61.4 ± 19 years, 56 male) were evaluated. Melanoma was the most prevalent diagnosis (51%), followed by non-small cell lung cancer (30%). ICI treatment consisted of PD-1, PDL-1 (nivolumab, pembrolizumab, atezolizumab), and CTLA-4 inhibitors (i) (ipilimumab) or combination PD-1i+CTLA4i. Renal toxicity developed after a median of four cycles of therapy. Fifty-one patients (65.5%) developed the most severe form of AKI- stage 3, including five patients requiring dialysis. All the 19 patients treated with dual ICI blockade developed AKI-stage 3, compared with 29 patients out of the 60 receiving a single agent (p<0.001). Most events were managed with corticosteroids associated with ICI withdrawal. In 15 patients ICI was restarted, but in six (40%) AKI recurred. Overall, 32 patients (40%) presented a complete renal recovery, which chance was inversely associated with dual ICI blockade (OR 0.15, 95CI 0.03-0.7, p=0.01). Conclusion: ICI-related ATIN may develop late after the therapy initiation, presenting as severe AKI, particularly in patients with dual ICI blockade. Although this complication may be partially reversible, concerns remain about the renal function sequelae and the possibility of restarting ICI treatment. [ABSTRACT FROM AUTHOR]

Background: We present two children with acute tubulointerstitial nephritis (ATIN) caused by leptospirosis in a 12-year-old boy and hantavirus in a 10-year-old girl. The role of glucocorticoids in the management of ATIN triggered by infectious agents is unclear. Case-diagnosis/treatment: Both children were hospitalized with jaundice, elevated serum creatinine, and thrombocytopenia. There was no oliguria or hypertension. Urine analysis revealed tubular proteinuria. Kidney biopsy was performed on one patient and showed tubulointerstitial inflammation with mild mesangial proliferation. Both patients were treated with glucocorticoids in view of deteriorating kidney function with respective serum creatinine values of 5.2 and 4.1 mg/dl. Both children exhibited an excellent clinical and biochemical response to treatment. Neither of the patients required dialysis. Positive serology test results indicated a recent leptospirosis and hantavirus infection. Conclusions: Leptospirosis and hantavirus associated ATIN share common clinical and biochemical features. Due to the low incidence in Europe these infectious causes of kidney dysfunction may be overlooked. Glucocorticoids may be considered in the management of ATIN. [ABSTRACT FROM AUTHOR]

Objective: To analyze the clinical and laboratory features of patients with acute tubulointerstitial nephritis (ATIN) and its differential diagnosis with acute tubular necrosis (ATN). Methods: From January 2009 to December 2018, patients with ATIN or ATN confirmed by renal biopsy in the Department of Nephrology, Ruijin Hospital ，Shanghai Jiao Tong Universtiy School of Medicine were included. The clinical manifestations and laboratory examination data were collected and analyzed comparatively. Results: During the period, there were 5 537 patients receiving renal biopsy,inclu-ding 135 ATIN cases [2.4% (135/5 537)] and 109 ATN [2.0%(109/5 537)].ATIN accounted for 21.4% (135/630) of the acute kidney disease (AKD) patients. The median age of ATIN patients was 53 years old and the female proportion was 57.0%. Main clinical manifestations of ATIN included fever, rash and arthralgia. Infection, and medicine use and toxic exposure were common inducements of ATIN. Compared with the ATN group, ATIN patients had higher female proportion (57.0% vs 33.9%) and lower BMI (22.9±3.6 vs 24.6±3.9, P

IntroductionAcute kidney injury (AKI) in cancer patients receiving immune checkpoint inhibitors (ICIs) may recognize multiple causes. Here, we reviewed cases of biopsy-proven acute tubulointerstitial nephritis (ATIN) to describe the clinical characteristics and outcomes of this condition.MethodWe conducted a pooled analysis of clinical cases of ICI-related biopsy-proven ATIN up to 1 May 2022. We collected data on clinical characteristics, AKI, biopsy findings, laboratory examinations, and renal outcomes.ResultsEighty-five patients (61.4 ± 19 years, 56 male) were evaluated. Melanoma was the most prevalent diagnosis (51%), followed by non-small cell lung cancer (30%). ICI treatment consisted of PD-1, PDL-1 (nivolumab, pembrolizumab, atezolizumab), and CTLA-4 inhibitors (i) (ipilimumab) or combination PD-1i+CTLA4i. Renal toxicity developed after a median of four cycles of therapy. Fifty-one patients (65.5%) developed the most severe form of AKI- stage 3, including five patients requiring dialysis. All the 19 patients treated with dual ICI blockade developed AKI-stage 3, compared with 29 patients out of the 60 receiving a single agent (p

Drug‐induced tubulointerstitial nephritis is an uncommon complication in patients on anti‐tuberculosis therapy that can lead to permanent kidney damage. Rifampicin is the most offending drug. We report a case of a 41‐years old man being treated for pulmonary tuberculosis and presenting with tubulointerstitial nephritis associated with rifampicin. We focus on diagnosis features and therapeutic challenges. [ABSTRACT FROM AUTHOR]

Abstract Background Cholesterol crystal embolization syndrome (CES) occurs when an atherosclerotic plaque causes small-vessel embolization, resulting in multi-organ damage. Although CES is pathologically characterized by an infiltration of eosinophils, the implication of the systemic inflammatory response represented by hypereosinophilia is unclear in clinical practice. Herein we present the case of a patient diagnosed with CES who developed multiple allergic organ injuries, including daptomycin-related dermatitis and later vancomycin-induced acute tubulointerstitial nephritis, which was successfully treated by the withdrawal of each medicine with or without corticosteroid therapy, one by one. Case presentation A 76-year-old Japanese man diagnosed with thoracic aneurysm rupture underwent total arch replacement through the open stent graft technique. Postoperatively, he developed methicillin-resistant Staphylococcus epidermidis bacteremia, which was treated with daptomycin. Subsequently, he presented with palpable purpura on both dorsal feet, erythema around his body, and hypereosinophilia. Daptomycin was replaced with vancomycin due to suspicion of drug-induced erythema. The erythema gradually faded. On nine days after vancomycin therapy, the systemic erythema rapidly reappeared followed by acute renal failure. The renal function decline prompted hemodialysis. A skin biopsy revealed cholesterol embolization, whereas a kidney biopsy revealed acute tubulointerstitial nephritis. After vancomycin discontinuation and initiation of systemic corticosteroid treatment, his kidney function was restored to the baseline level. Conclusions The present case highlights cholesterol embolization can cause allergic complications in addition to direct organ damage.

Abstract Drug‐induced tubulointerstitial nephritis is an uncommon complication in patients on anti‐tuberculosis therapy that can lead to permanent kidney damage. Rifampicin is the most offending drug. We report a case of a 41‐years old man being treated for pulmonary tuberculosis and presenting with tubulointerstitial nephritis associated with rifampicin. We focus on diagnosis features and therapeutic challenges.

Introduction: Acute tubulointerstitial nephritis (ATIN) is a well-recognized cause of acute kidney injury (AKI) due to the tubulointerstitial inflammation. The aim of this study was to explore the clinical features, outcomes, and responses to corticosteroid treatment in patients with ATIN. Methods: Patients with biopsy-proven ATIN, who were diagnosed between 1994 and 2016 at the Department of Nephrology, Charles University, First Faculty of Medicine, and General University Hospital in Prague, were included in the study. Patient demographics, the aetiological and clinical features, the treatment given, and the outcome at 1 year of follow-up were extracted from patient records. Results: A total of 103 ATIN patients were analysed, of which 68 had been treated with corticosteroids. There was no significant difference in the median serum creatinine 280 (169–569) µmol/L in the conservatively managed group versus 374 (249–558) µmol/L in the corticosteroid-treated group, p = 0.18, and dependence on dialysis treatment at baseline at the time of biopsy (10.3 vs. 8.6%). During the 1 year of follow-up, those ATIN patients who had been treated with corticosteroids did better and showed greater improvement in kidney function, determined as serum creatinine difference from baseline and from 1 month over 1-year period (p = 0.001). Conclusions: This single-centre retrospective cohort study supports the beneficial role of the administration of corticosteroid therapy in the management of ATIN.

The COVID-19 pandemic caused by coronavirus SARS-CoV-2 is currently a main public health problem worldwide. The clinical symptoms relate primarily to the respiratory system but may also involve multiple organs. The course of COVID-19 in children is usually mild, but in some cases may cause late complications, particularly the pediatric inflammatory multisystem syndrome (PIMS-TS). One of its symptoms may be acute kidney injury. We present a 10-year-old boy who developed nonspecific symptoms a few weeks after mild COVID-19, including weakness, weight loss, and polyuria. Clinical evaluation revealed acute renal failure secondary to acute tubulointerstitial nephritis (ATIN). Treatment with glucocorticoids resulted in rapid clinical and laboratory improvement. We hypothesize that the development of ATIN could be causally related to COVID-19 in an immune pathomechanism similar to PIMS-TS. The case provides new insights into possible complications of SARS-CoV-2 infection and indicates the need for renal follow-up after COVID-19.

The introduction of immune checkpoint inhibitors (ICI) has resulted in significant improvement in cancer care, but has been accompanied by the occurrence of immune-related adverse events (irAEs). Also, kidney irAEs have been reported, and the most frequent one is acute tubulointerstitial disease which impacts renal and overall prognosis. There is an unmet need to stratify renal risk in oncologic patients, to allow individualized monitoring and therefore, early detection of ICI-related acute kidney injury (ICI-AKI). Although risk factors for ICI-AKI have been described in previous case–control studies, where 'cases' were ICI-AKI patients and 'controls' ICI-treated patients without AKI, there is limited epidemiologic knowledge concerning patients developing different irAEs. In this issue of the Clinical Kidney Journal , Gerard et al. describe five factors that were associated with the development of ICI-AKI: older age, previous chronic kidney disease, and concomitant use of fluindione, non-steroidal anti-inflammatory drugs and proton pump inhibitors. These findings suggest that ICI may be a 'second hit' that precipitates AKI caused by a concomitant drug. These results urge an increased focus to prevent the prescription of potential nephrotoxic drugs in ICI-treated patients, avoiding iatrogenic events. [ABSTRACT FROM AUTHOR]

Background: Cholesterol crystal embolization syndrome (CES) occurs when an atherosclerotic plaque causes small-vessel embolization, resulting in multi-organ damage. Although CES is pathologically characterized by an infiltration of eosinophils, the implication of the systemic inflammatory response represented by hypereosinophilia is unclear in clinical practice. Herein we present the case of a patient diagnosed with CES who developed multiple allergic organ injuries, including daptomycin-related dermatitis and later vancomycin-induced acute tubulointerstitial nephritis, which was successfully treated by the withdrawal of each medicine with or without corticosteroid therapy, one by one.Case Presentation: A 76-year-old Japanese man diagnosed with thoracic aneurysm rupture underwent total arch replacement through the open stent graft technique. Postoperatively, he developed methicillin-resistant Staphylococcus epidermidis bacteremia, which was treated with daptomycin. Subsequently, he presented with palpable purpura on both dorsal feet, erythema around his body, and hypereosinophilia. Daptomycin was replaced with vancomycin due to suspicion of drug-induced erythema. The erythema gradually faded. On nine days after vancomycin therapy, the systemic erythema rapidly reappeared followed by acute renal failure. The renal function decline prompted hemodialysis. A skin biopsy revealed cholesterol embolization, whereas a kidney biopsy revealed acute tubulointerstitial nephritis. After vancomycin discontinuation and initiation of systemic corticosteroid treatment, his kidney function was restored to the baseline level.Conclusions: The present case highlights cholesterol embolization can cause allergic complications in addition to direct organ damage. [ABSTRACT FROM AUTHOR]

Novel coronavirus disease infection (coronavirus disease 2019, COVID-19) was declared a global pandemic in March 2020 and since then has become a major public health problem. The prevalence of COVID-19 infection and acute kidney injury (AKI) is variable depending on several factors such as race/ethnicity and severity of illness. The pathophysiology of renal involvement in COVID-19 infection is not entirely clear, but it could be in part explained by the viral tropism in the kidney parenchyma. AKI in COVID-19 infection can be either by direct invasion of the virus or as a consequence of immunologic response. Diverse studies have focused on the effect of COVID-19 on glomerulonephritis (GN) patients or the 'novo' GN; however, the effect of COVID-19 in acute tubulointerstitial nephritis (ATIN) has been scarcely studied. In this article, we present five cases with different spectrums of COVID-19 infection and ATIN that may suggest that recent diagnosis of ATIN is accompanied by a worse clinical prognosis in comparison with long-term diagnosed ATIN. [ABSTRACT FROM AUTHOR]

Abstract Background Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis usually induces rapidly progressive glomerulonephritis, including pauci-immune necrotizing crescentic glomerulonephritis. Acute tubulointerstitial nephritis (ATIN), which is often drug-induced, is a frequent cause of kidney injury. However, ATIN associated with ANCA without any glomerular lesions has been rarely reported, and drug-induced ATIN associated with ANCA is not well recognized. Here we present a case of an older woman with ATIN associated with myeloperoxidase-ANCA (MPO-ANCA) following cimetidine treatment. Case presentation A 70-year-old woman was admitted to our hospital due to acute kidney injury and mild proteinuria. She had a one-year history of chronic thyroiditis and dyslipidemia, for which she was taking levothyroxine sodium and atorvastatin, respectively. Two weeks before admission she had started cimetidine, methylmethionine sulfonium chloride, and itopride hydrochloride for gastric discomfort persistent since a month. She had experienced fatigue for two weeks and later appetite loss. The patient demonstrated a positive titer for MPO-ANCA (192 IU/mL) and a positive drug-induced lymphocyte stimulation test for cimetidine. She underwent two kidney biopsies that revealed ATIN without any glomerular lesions. Despite discontinuation of cimetidine on admission, renal injury continued with the presence of high MPO-ANCA titer. Oral steroid treatment was closely related with the recovery of her renal function and disappearance of MPO-ANCA. Conclusions In this case, ATIN presented as sustained renal insufficiency and high MPO-ANCA titer despite withdrawal of cimetidine. Therefore, we reason that the development of ANCA-associated ATIN was caused by cimetidine. Serologic follow-up with measurement of MPO-ANCA titers and renal biopsy are recommended when the clinical history is inconsistent with the relatively benign course of drug-induced ATIN.

Antineutrophilic cytoplasmic antibody (ANCA) has been reported to be associated with systemic vasculitis. However, there are few reports regarding ATIN and ANCA without drug involvement. In this article, we present a case of ATIN with a high titre of ANCA, without systemic disease or any responsible drug. Here we present a case of A 41 year female, p/w breathlessness at rest, decreased urine output, fever and anorexia for 10 days. She had no other significant medical illness. Laboratory investigations were done where creatinine, urea, potassium levels and ESR were significantly raised and urine analysis showed proteinuria. RA Factor, ANA titre and C-ANCA were positive. Kidneys on USG s/o B/L increase in echogenicity with normal size and preserved CMD. Percutaneous Renal biopsy performed showed tubular atrophy with few foci of lymphocytic tubulitis and focal intratubular neutrophilic casts. Interstitium shows patchy moderate mixed inflammatory infiltrates. Emergency HD was done on admission followed by pulse therapy of Methyl prednisone after which her renal function improved and patient got better and was subsequently discharged on oral prednisone. ATIN is a relatively rare pathologic finding among ANCArelated renal injury. ATIN can be associated with positive ANCA without features of renal limited vasculitis or systemic vasculitis and can also occur in absence of drug exposure. [ABSTRACT FROM AUTHOR]

Background and Objectives: In clinical practice, some patients are diagnosed with diabetic nephropathy (DN) combined with acute tubulointerstitial nephritis (ATIN) through renal biopsy. There is relatively little research on the treatment and prognosis of such patients, and no consensus exists on the use of glucocorticoid for treatment. Therefore, our study explores the progression of DN combined with ATIN and the renal outcomes after treatment with glucocorticoid., Methods: This study retrospectively analyzed patients diagnosed with DN combined with ATIN through renal biopsy at our center from January 1, 2015, to December 31, 2021. We collected general patient information, laboratory indicators, renal pathology indicators, and the glucocorticoid usage after kidney biopsy. Follow-up data were collected from medical records. Statistical analysis methods included t-tests, non-parametric tests, and chi-square tests. Univariate and multivariate Cox regression analyses were used to evaluate the risk factors for renal endpoint events in patients. Statistical significance was defined as p -values < 0.05., Results: In this study, a total of 67 patients were included. The subjects were divided into two groups based on whether they received glucocorticoid treatment: 33 patients in the steroid group and 34 in the non-steroid group. In the steroid group, 19 patients reached the renal endpoint event, which was significantly higher than in the non-steroid group (57.58% vs. 29.41%, p  = 0.038). Univariate Cox regression analysis showed that serum creatinine (HR = 1.008, p  < 0.001), albumin (HR = 0.919, p  < 0.001), 24-h urinary protein (HR = 1.093, p  = 0.002), hemoglobin (HR = 0.964, p  = 0.001), triglycerides (HR = 1.12, p  = 0.04), and the use of glucocorticoid (HR = 2.507, p  = 0.019) were influencing factors for renal endpoint events in patients with DN combined with ATIN. Multivariate Cox regression analysis showed that albumin (HR = 0.863, p  = 0.003) was an independent risk factor for renal endpoint events in patients with DN combined with ATIN., Conclusions: The use of glucocorticoid in treatment does not improve renal prognosis in patients with DN combined with ATIN. Lower levels of albumin are associated with a worse renal prognosis.

Introduction Acute tubulointerstitial nephritis (ATIN) is a common cause of acute kidney injury with various etiologies. It has been shown that autoimmune-related ATIN (AI-ATIN) has a higher recurrence rate and a greater likelihood of developing into chronic kidney disease compared with drug-induced ATIN, yet misdiagnosis at renal biopsy is not uncommon. Methods Patients who were clinicopathologically diagnosed as ATIN from January 2006 to December 2015 in Peking University First Hospital were enrolled. Clinical, pathological and follow-up data were collected. Serum samples on the day of renal biopsy were collected and tested for anti-C-reactive protein (CRP) antibodies. CRP and its linear peptides were used as coating antigens to detect antibodies. Statistical analysis was used to assess the diagnostic value of the antibodies. Results Altogether 146 patients were enrolled. The receiver operating characteristic–area under the curve of the anti-CRP antibody for the identification of late-onset AI-ATIN was 0.750 (95% confidence interval 0.641–0.860, P < 0.001) and the positivity was associated with ATIN relapse (adjusted hazard ratio = 4.321, 95% confidence interval 2.402–7.775, P < 0.001). Antibodies detected by CRP linear peptide 6 (PT6) were superior with regard to differentiating patients with AI-ATIN, while antibodies detected by peptide 17 (PT17) could predict ATIN relapse. Antibodies detected by these two peptides were positively correlated with the severity of tubular dysfunction and pathological injury. Conclusions Serum anti-CRP antibody could be used to differentiate late-onset AI-ATIN and predict relapse of ATIN at the time of renal biopsy. The CRP linear peptides PT6 and PT17 could be used as coating antigens to detect anti-CRP antibodies, which may provide more information for the clinical assessment of ATIN. [ABSTRACT FROM AUTHOR]

Immune checkpoint inhibitors (ICIs) are nowadays widely used in clinical oncology treatment, and significantly improve the prognosis of cancer patients. However, overactivation of T cells and related signaling pathways caused by ICIs can also induce immune‐related adverse effects (irAEs). Renal immune side‐effects are relatively rare, but some are serious and fatal. Acute kidney injury (AKI), diagnosed mainly by percentage increases in serum creatinine (sCr), is the most common clinical manifestation, while acute tubulointerstitial nephritis (ATIN) is the main cause of ICI‐related AKI. Urinalysis analysis and sediment evaluation, 24 hour urine protein and sCr are helpful in screening and monitoring renal irAEs. Multiple potential causes for AKI are involved during cancer therapy, and should be differentiated from the immune mechanisms of ICIs. Under these circumstances, a renal biopsy should be considered which is essential for clinical decision‐making. Steroids are an effective treatment option for renal irAEs. Most patients who experience ICI‐related ATIN achieve a partial or complete renal recovery with prompt diagnosis and treatment. Multidisciplinary collaborations of different specialists will improve the effectiveness and outcome in the management of ICI irAEs.

Background: The syndrome of tubulointerstitial nephritis and uveitis (TINU) is an uncommon and multisystemic autoimmune disorder. This review reports a rare case of TINU being superimposed on thrombotic microangiopathy (TMA) and, by comparing with the available literature, also summarizes the clinical features, associated conditions, treatment, and outcome of patients with TINU. Summary: Herein, we report the case of a 37-year-old male patient with acute kidney injury (AKI) clinicopathologically identified as malignant hypertension-induced TMA superimposed by acute tubulointerstitial nephritis, which was suspected to be related to drug hypersensitivity. After treatment with oral prednisone combined with a renin-angiotensin system inhibitor, the patient achieved partial renal recovery and was withdrawn from hemodialysis. Recurrent AKI concomitant with new-onset asymptomatic uveitis was detected during routine clinical follow-up after cessation of prednisone. TINU was then diagnosed, and prednisone followed by cyclophosphamide was prescribed. The patient achieved better renal recovery than in the first round of treatment and maintained stable renal function afterward. By reviewing the literature, 36 cases were reported as TINU superimposed on other conditions, including thyroiditis, osteoarthropathy, and sarcoid-like noncaseating granulomas. Key messages: TINU could be complicated by many other conditions, among which TMA is very rare. When presented as AKI, kidney biopsy is important for differential diagnosis. The case also shows that recurrent AKI with concomitant uveitis after prednisone withdrawal strongly suggested the need for long-term follow-up and elongated prednisone therapy for TINU syndrome.

Background Glycosuria is one of the manifestations of acute tubulointerstitial nephritis (ATIN), but may also be observed in other renal diseases. In this study, we investigated the value of non-diabetic glycosuria as a diagnostic clue for ATIN. Methods We retrospectively reviewed the medical records of adult patients who underwent a kidney biopsy as an evaluation for serum creatinine > 1.4 mg/dL. Patients with proteinuria in the nephrotic range, diabetes mellitus, or transplanted kidney were excluded. The laboratory abnormalities suggestive of tubular injury were compared between 28 patients (14 men and 14 women, mean age 48.5 ± 14.1 years) with ATIN and 116 patients (76 men and 40 women, mean age 53.1 ± 15.0 years) with other diagnoses. Results In ATIN, glycosuria (≥ 1+ on dipstick; 68%) was more frequent than hypophosphatemia (18%), hypouricemia (18%), hypokalemia (18%), and tubular proteinuria (40%). In other diagnoses, glycosuria (≥ 1+) was detected in 7 (6%) patients; 6 of them had the histological diagnosis of antineutrophil cytoplasmic antibody-associated glomerulonephritis. The presence of glycosuria (≥ 1+) had 68% sensitivity and 94% specificity for ATIN, with the positive likelihood ratio of 11.24 and the negative likelihood ratio of 0.34. Pyuria and low total CO2 were equally and more sensitive (68% and 71%, respectively) than glycosuria (≥ 1+), but had no diagnostic value due to low specificities (58% and 60%, respectively). Conclusion In non-diabetic, non-nephrotic patients undergoing a kidney biopsy for azotemia, 1+ or higher glycosuria, if present, was a good predictor of the diagnosis of ATIN.

Coronavirus disease 2019 (COVID-19) is an ongoing pandemic that to date has spread to >100 countries. Acute kidney injury is not uncommon with this disease. The most common kidney biopsy finding is acute tubular injury. Glomerular diseases such as collapsing glomerulopathy and vasculitis, and thrombotic microangiopathy have been reported. Viral inclusion particles with distinctive spikes in the tubular epithelium and podocytes, and endothelial cells of the glomerular capillary loops, have been visualized by electron microscopy by some but disputed by others as non-viral structures. Interstitial infiltrates have not commonly been described in the published kidney biopsy series from patients with COVID-19. Medications used to treat COVID-19 can lead to interstitial nephritis, but very few have been reported. In summary, interstitial kidney disease is a rare finding in COVID-19. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic caused by coronavirus SARS-CoV-2 is currently a main public health problem worldwide. The clinical symptoms relate primarily to the respiratory system but may also involve multiple organs. The course of COVID-19 in children is usually mild, but in some cases may cause late complications, particularly the pediatric inflammatory multisystem syndrome (PIMS-TS). One of its symptoms may be acute kidney injury. We present a 10-year-old boy who developed nonspecific symptoms a few weeks after mild COVID-19, including weakness, weight loss, and polyuria. Clinical evaluation revealed acute renal failure secondary to acute tubulointerstitial nephritis (ATIN). Treatment with glucocorticoids resulted in rapid clinical and laboratory improvement. We hypothesize that the development of ATIN could be causally related to COVID-19 in an immune pathomechanism similar to PIMS-TS. The case provides new insights into possible complications of SARS-CoV-2 infection and indicates the need for renal follow-up after COVID-19. [ABSTRACT FROM AUTHOR]

Acute kidney injury related to rifampin is usually a clinical diagnosis. We report a case of a man being treated for pulmonary tuberculosis with acute tubulointerstitial nephritis related to rifampicin.

Background: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis usually induces rapidly progressive glomerulonephritis, including pauci-immune necrotizing crescentic glomerulonephritis. Acute tubulointerstitial nephritis (ATIN), which is often drug-induced, is a frequent cause of kidney injury. However, ATIN associated with ANCA without any glomerular lesions has been rarely reported, and drug-induced ATIN associated with ANCA is not well recognized. Here we present a case of an older woman with ATIN associated with myeloperoxidase-ANCA (MPO-ANCA) following cimetidine treatment.Case Presentation: A 70-year-old woman was admitted to our hospital due to acute kidney injury and mild proteinuria. She had a one-year history of chronic thyroiditis and dyslipidemia, for which she was taking levothyroxine sodium and atorvastatin, respectively. Two weeks before admission she had started cimetidine, methylmethionine sulfonium chloride, and itopride hydrochloride for gastric discomfort persistent since a month. She had experienced fatigue for two weeks and later appetite loss. The patient demonstrated a positive titer for MPO-ANCA (192 IU/mL) and a positive drug-induced lymphocyte stimulation test for cimetidine. She underwent two kidney biopsies that revealed ATIN without any glomerular lesions. Despite discontinuation of cimetidine on admission, renal injury continued with the presence of high MPO-ANCA titer. Oral steroid treatment was closely related with the recovery of her renal function and disappearance of MPO-ANCA.Conclusions: In this case, ATIN presented as sustained renal insufficiency and high MPO-ANCA titer despite withdrawal of cimetidine. Therefore, we reason that the development of ANCA-associated ATIN was caused by cimetidine. Serologic follow-up with measurement of MPO-ANCA titers and renal biopsy are recommended when the clinical history is inconsistent with the relatively benign course of drug-induced ATIN. [ABSTRACT FROM AUTHOR]

A 16-year-old boy presented with uveitis in both eyes with recurrent febrile illness and renal ailments. The patient was referred to a nephrologist. Subsequent investigations revealed acute tubulointerstitial nephritis in a renal biopsy and raised urinary beta-2 microglobulin (B2M). Based on his clinical findings and laboratory investigations, a diagnosis of tubulointerstitial nephritis and uveitis (TINU) syndrome was made. Since, the literature on TINU through India is sparse, the two available case reports were published through nephrology setup. Our case illustrates how ophthalmologist can aid in the diagnosis of such a rare clinical entity using interdisciplinary approach.

Immune checkpoint inhibitors (ICIs) have been used more and more Increasingly in clinical oncology treatment, which has significantly improved the prognosis of cancer patients. Over-activation of T cells and related signaling pathways may cause immune-related adverse effects. Renal immune side-effects are relatively rare, but some of them are serious and fatal. This review analyses of the Incidence, clinical and pathological manifestations of ICIs-induced renal injury, and focuses on the differential diagnosis and treatment. Because there are many secondary factors that need to be differentiated from immune mechanism, renal biopsy should be performed if necessary to determine the important decision.

Abstract Background Acute tubulointerstitial nephritis (ATIN) is an important cause of acute kidney injury and often a potentially reversible disease. However, the role of steroids in ATIN remains controversial and the underlying mechanisms remain unresolved. Methods A total of 113 adult patients with biopsy-proven ATIN were recruited from three tertiary referral centers. Of 102 patients with idiopathic or drug-induced ATIN, outcomes such as renal recovery, end-stage renal disease, and all-cause mortality were compared between the steroid-treated and non-treated groups. Plasma and urine inflammatory cytokine levels at the time of biopsy were analyzed in patients (n = 33) using a bead-based multiplex assay and compared with those of healthy individuals (n = 40). Results Steroids were used in 92 (81.4%) of the total patients and in 82 (80.3%) patients with idiopathic or drug-induced ATIN. The rate of renal recovery and the risks of end-stage renal disease and mortality were not different between the steroid-treated and non-treated groups. Despite using a propensity score matching method (n = 20 in each group), none of the outcomes were different between the two groups. Several cytokines, such as monocyte chemotactic protein-1, interferon-α, and interleukin-6 and interleukin-8 levels, were markedly elevated in plasma and urine of patients compared with those in healthy individuals. However, cytokines related to Th2 response, such as IL-10, IL-33, were not different between the two groups. Conclusions Steroid use does not affect the overall outcome of ATIN. Based on the fact that targeting therapy should be investigated to improve outcomes, the present cytokine results will be helpful for developing a novel therapy for ATIN.

Abstract Rationale & Objective The approved therapeutic indication for immune checkpoint inhibitors (CPIs) are rapidly expanding including treatment in the adjuvant setting, the immune related toxicities associated with CPI can limit the efficacy of these agents. The literature on the nephrotoxicity of CPI is limited. Here, we present cases of biopsy proven acute tubulointerstitial nephritis (ATIN) and glomerulonephritis (GN) induced by CPIs and discuss potential mechanisms of these adverse effects. Study design, setting, & participants We retrospectively reviewed all cancer patients from 2008 to 2018 who were treated with a CPI and subsequently underwent a kidney biopsy at The University of Texas MD Anderson Cancer Center. Results We identified 16 cases diagnosed with advanced solid or hematologic malignancy; 12 patients were male, and the median age was 64 (range 38 to 77 years). The median time to developing acute kidney injury (AKI) from starting CPIs was 14 weeks (range 6–56 weeks). The average time from AKI diagnosis to obtaining renal biopsy was 16 days (range from 1 to 46 days). Fifteen cases occurred post anti-PD-1based therapy. ATIN was the most common pathologic finding on biopsy (14 of 16) and presented in almost all cases as either the major microscopic finding or as a mild form of interstitial inflammation in association with other glomerular pathologies (pauci-immune glomerulonephritis, membranous glomerulonephritis, C3 glomerulonephritis, immunoglobulin A (IgA) nephropathy, or amyloid A (AA) amyloidosis). CPIs were discontinued in 15 out of 16 cases. Steroids and further immunosuppression were used in most cases as indicated for treatment of ATIN and glomerulonephritis (14 of 16), with the majority achieving complete to partial renal recovery. Conclusions Our data demonstrate that CPI related AKI occurs relatively late after CPI therapy. Our biopsy data demonstrate that ATIN is the most common pathological finding; however it can frequently co-occur with other glomerular pathologies, which may require immune suppressive therapy beyond corticosteroids. In the lack of predictive blood or urine biomarker, we recommend obtaining kidney biopsy for CPI related AKI.

Chemotherapy-associated renal injury is considered one of the major concerns among nephrological and oncological practice. The use of novel anti-neoplastic therapies that target carcinomas has helped in the detection of this form of renal injury. Immune checkpoint inhibitors (ICPIs) are a group of monoclonal antibodies targeting inhibitory receptors that exist on tumor cells and T cells. ICPIs are able to suppress tumors that might have escaped from the immune surveillance. Meanwhile, although ICPIs have shown promising efficacy in cancer treatment, their immune-related side effects limit their widespread use in cancer therapy schedules. One of the major side effects limiting ICPIs’ usage is nephrotoxicity. Glomerular disease, acute interstitial nephritis (AIN), and acute tubular necrosis (ATN) are considered different infusion-related adverse events. Infiltration of eosinophils, T lymphocytes, and plasma cells, as well as interstitial inflammation and edema, leading to acute tubulointerstitial nephritis (ATIN). It is conceivable that the rupture of self-tolerance by ICPIs induces an autoimmune reaction against some specific self-antigens in the organs including kidneys. The exact nature of the antigen is unclear; however, it is possible that it is found in the renal tubular cells, as indicated by a greater frequency of ATIN in kidney biopsies. The current review paper discusses the relationship between ICPIs therapy and kidney disorders or more specifically, their possible role in renal damage along with renal toxicity profile in the setting of ICPIs treatment.

Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment since their introduction ∼15 years ago. However, these monoclonal antibodies are associated with immune-related adverse events that can also affect the kidney, resulting in acute kidney injury (AKI), which is most commonly due to acute tubulointerstitial nephritis (ATIN). Limited data are available on the true occurrence of ICI-associated AKI. Furthermore, evidence to guide the optimal management of ICI-associated AKI in clinical practice is lacking. In this issue, Oleas et al. report a single-center study of patients with nonhematologic malignancies who received ICI treatment during a 14-month period, experienced AKI and underwent a kidney biopsy at the Vall d'Hebron University Hospital. Importantly, they demonstrate that only a minority of ICI-associated AKI patients was referred to the nephrology service and kidney biopsy was only performed in 6.4% of patients. Although the authors add to our knowledge about ICI-associated AKI, their article also highlights the need for the development of noninvasive diagnostic markers for ICI-associated ATIN, the establishment of treatment protocols for ICI-associated ATIN and recommendations for optimal ICI rechallenge in patients with previous ICI-associated AKI. [ABSTRACT FROM AUTHOR]

Acute drug-allergic tubulointerstitial nephrites are increasingly common conditions in current practice due to increased patient access to a variety of drugs. The clinical-biological panel associates acute renal injury with hypersensitivity phenomena. Considered classically reversible after the cessation of the incriminated drug, drug-allergic tubulointerstitial nephrites have changed their evolutionary characteristics in recent decades, even under treatment. This article presents the clinical-biological, therapeutic and evolutionary characteristics of drug-allergic tubulointerstitial nephrites. [ABSTRACT FROM AUTHOR]

Abstract Background We previously described an endogamous Pakistani kindred in whom we identified a novel homozygous missense mutation in the PRKCD gene encoding for protein kinase C δ (PKCδ) as a cause of monogenic systemic lupus erythematosus (SLE). PKCδ has a role in the negative regulation of B cells. Given the nature of the disease, a logical targeted therapeutic approach in these patients is B cell depletion. Indeed, the 3 siblings all had a marked clinical response and resolution of symptoms with rituximab, although 2 of the siblings had severe reactions to rituximab thus precluding further treatment with this. We therefore describe the first successful use of ofatumumab for this rare form of monogenic SLE. Case presentation All three affected siblings presented with SLE before the age of 3-years with lethargy, intermittent fever, thrombocytopenia, cutaneous involvement, alopecia, and hepatosplenomegaly. Tubulointerstitial nephritis was also present in 1 of the siblings. Homozygosity mapping followed by whole exome sequencing identified a homozygous missense mutation in PRKCD (p.Gly432Trp), subsequently confirmed by Sanger sequencing to be present in all 3 siblings. All 3 patients were initially treated with rituximab, however 2 of the siblings developed severe infusion-related reactions. For subsequent disease flare in these individuals we therefore used an alternative B cell depleting agent, ofatumumab (300 mg/1.73m2 on day 1; 700 mg/1.73m2 on day 15). This resulted in marked clinical improvement in both patients. To the best of our knowledge, this is the first report describing the successful use of ofatumumab for PKCδ deficiency. Conclusions PKCδ deficiency causes a monogenic form of SLE which responds well to B cell depletion. Ofatumumab is also likely to have a therapeutic role for sporadic juvenile SLE (jSLE) patients intolerant of rituximab.

Abstract Background Cilostazol is an antiplatelet drug that is widely prescribed for the prevention of secondary stroke. Adverse reactions to cilostazol include headaches, palpitations, and diarrhea. Little is known about the nephrotoxicity of cilostazol, such as acute kidney injury. We report a biopsy-proven case of diffuse tubulointerstitial nephritis induced by cilostazol. Case presentation A 69-year-old woman prescribed cilostazol was hospitalized for acute kidney injury. On admission, her renal function deteriorated, with an increased serum creatinine level. Urinalysis showed hematuria, proteinuria, and hyper-beta2-microglobulinuria. A renal biopsy revealed diffuse tubulointerstitial nephritis associated with IgA nephropathy, and gallium-67 scintigraphy showed uptake in the bilateral kidneys. A drug lymphocyte stimulation test for cilostazol was positive, and the patient was diagnosed with cilostazol-induced acute tubulointerstitial nephritis. Despite discontinuation of cilostazol, her renal function rapidly worsened and steroid pulse therapy was initiated, followed by oral high-dose glucocorticoid therapy. After steroid treatment, her serum creatinine level normalized in parallel with urine beta2-microglobulin. Conclusion Cilostazol can induce acute tubulointerstitial nephritis.

Abstract Background Acute tubulointerstitial nephritis (ATIN) has been increasingly recognized as an important manifestation of kidney injury associated with the use of immune checkpoint inhibitors (anti-PD-1 and anti-CTLA-4). While the exact pathophysiology remains unknown, corticosteroids are the mainstay of management. Case presentation We describe a 67-year-old man with stage IV non-small-cell lung cancer who developed kidney injury during treatment with the anti-PD-1 antibody nivolumab. A kidney biopsy showed ATIN without granuloma formation. Considering their mechanism of action, immune checkpoint inhibitors can alter immunological tolerance to concomitant drugs that have been safely used for a long time. For more than 4 years before the initiation of nivolumab therapy, the patient had been receiving the proton pump inhibitor lansoprazole, known to cause drug-induced ATIN, without significant adverse events including kidney injury. He showed rapid improvement in kidney function in 3 days (creatinine decreased from 2.74 to 1.82 mg/dl) on discontinuation of lansoprazole. He then received 500 mg intravenous methylprednisolone for 3 days followed by 1 mg/kg/day oral prednisolone and his creatinine levels eventually stabilized around 1.7 mg/dl. Drug-induced lymphocyte stimulation test (DLST) for lansoprazole was positive. Conclusions The rapid improvement of kidney function after discontinuation and DLST positivity indicate that lansoprazole contributed to the development of ATIN during nivolumab therapy. Considering the time course, it is plausible that nivolumab altered the long-lasting immunological tolerance against lansoprazole in this patient. To the best of our knowledge, this is the first case report of DLST positivity for a drug that had been used safely before the initiation of an immune checkpoint inhibitor. Although corticosteroid therapy is recommended, the recognition and discontinuation of concomitant drugs, especially those known to induce ATIN, is necessary for the management of kidney injury associated with anti-PD-1 therapy.

Currently, medications have the leading position in the development of acute tubulointerstitial nephritis. Antibiotics, proton pump inhibitors and non-steroidal anti-inflammatory drugs are the most common etiologic agents of acute tubulointerstitial nephritis. Various drugs produce ambiguous types of immune response. For instance, antibiotics may induce a systemic allergic reaction, including fever, skin rash, eosinophilia and arthralgia, whereas non-steroidal anti-inflammatory drugs and proton pump inhibitors may evoke a subclinical cell-modified response. Blood and urine tests, as well as renal ultrasound examination do not allow establishing a highly reliable diagnosis of acute tubulointerstitial nephritis. Therefore, renal biopsy is essential for the diagnosis. Morphological abnormalities include interstitial inflammation and tubulitis. In a patient who is on any medication and is having high serum creatinine levels, decreased glomerular filtration rate, and urine test abnormalities, the possibility of acute tubulointerstitial nephritis should be considered by the clinician; the disease can manifest at various time intervals after intake of the drug (from several days to months). Treatment approach is based first of all on immediate withdrawal of the nephrotoxic agent and possible administration of immunosuppressive therapy. Timely diagnosis and early administration of glucocorticoids in morphologically confirmed tubulointerstitial nephritis are critical for restoration of the kidney functioning. Chronic kidney disease can develop in some patients. Clinicians in any specialty have to know about potential negative consequences of the use of antibiotics, non-steroidal anti-inflammatory drugs, proton pump inhibitors and other medications and to consider nephrotoxic factors.

Glycosuria is one of the manifestations of acute tubulointerstitial nephritis (ATIN), but may also be observed in other renal diseases. In this study, we investigated the value of non-diabetic glycosuria as a diagnostic clue for ATIN. We retrospectively reviewed the medical records of adult patients who underwent a kidney biopsy as an evaluation for serum creatinine > 1.4 mg/dL. Patients with proteinuria in the nephrotic range, diabetes mellitus, or transplanted kidney were excluded. The laboratory abnormalities suggestive of tubular injury were compared between 28 patients (14 men and 14 women, mean age 48.5 ± 14.1 years) with ATIN and 116 patients (76 men and 40 women, mean age 53.1 ± 15.0 years) with other diagnoses. In ATIN, glycosuria (≥ 1+ on dipstick; 68%) was more frequent than hypophosphatemia (18%), hypouricemia (18%), hypokalemia (18%), and tubular proteinuria (40%). In other diagnoses, glycosuria (≥ 1+) was detected in 7 (6%) patients; 6 of them had the histological diagnosis of antineutrophil cytoplasmic antibody-associated glomerulonephritis. The presence of glycosuria (≥ 1+) had 68% sensitivity and 94% specificity for ATIN, with the positive likelihood ratio of 11.24 and the negative likelihood ratio of 0.34. Pyuria and low total CO2 were equally and more sensitive (68% and 71%, respectively) than glycosuria (≥ 1+), but had no diagnostic value due to low specificities (58% and 60%, respectively). In non-diabetic, non-nephrotic patients undergoing a kidney biopsy for azotemia, 1+ or higher glycosuria, if present, was a good predictor of the diagnosis of ATIN. [ABSTRACT FROM AUTHOR]