Diagnosis Of Acute Interstitial Nephritis Research Articles

Urine Eosinophils (UEs) Have No Practical Value for the Diagnosis of Acute Interstitial Nephritis (AIN)

Urine Eosinophils (UEs) Have No Practical Value for the Diagnosis of Acute Interstitial Nephritis (AIN)

Acute and Chronic Tubulointerstitial Nephritis of Rheumatic Causes.

Tubulointerstitial nephritis (TIN) is the second most common cause of acute intrinsic kidney injury after acute tubular necrosis. Although drug-induced forms of TIN represent the vast majority, rheumatic disease is another common cause and often underdiagnosed. Early diagnosis of acute interstitial nephritis and prompt withdrawal of the culprit medication or a correct treatment can avoid chronic damage and progressive chronic kidney disease. This review highlights the recent updates, clinical features, and treatment in TIN in autoimmune rheumatic disease.

Clinical Manifestations and Outcomes of Fluoroquinolone-Related Acute Interstitial Nephritis

ObjectiveTo describe the clinical presentation, diagnosis, and outcomes of patients with biopsy-proven acute interstitial nephritis (AIN) related to fluoroquinolone (FQ) therapy. Patient and MethodsWe conducted a retrospective review of biopsy-proven AIN attributed to FQ use at Mayo Clinic's campus in Rochester, Minnesota, from January 1, 1993, through December 31, 2016. Cases were reviewed by a renal pathologist and attributed to FQ use by an expert nephrologist. We also reviewed and summarized all published case reports of biopsy-proven AIN that were attributed to FQ use. ResultsWe identified 24 patients with FQ-related biopsy-proven AIN at our institution. The most commonly prescribed FQ was ciprofloxacin in 17 patients (71%), and the median antibiotic treatment duration was 7 days (interquartile range [IQR], 5-12 days). The median time from the initiation of FQ to the diagnosis of AIN was 8.5 days (IQR, 3.75-20.75 days). Common clinical manifestations included fever (12; 50%), skin rash (5; 21%), and flank pain (2; 8%), and 9 (38%) had peripheral eosinophilia. However, 4 (17%) of the patients were asymptomatic at the time of diagnosis and AIN was suspected on the basis of routine laboratory monitoring. Most patients (17; 71%) recovered after the discontinuation of antibiotic therapy, and renal function returned to baseline at a median of 20.5 days (IQR, 11.75-27.25 days). Six patients (25%) required temporary hemodialysis, and 14 patients (58%) received corticosteroid therapy. ConclusionThe onset of FQ-related AIN can be delayed, and a high index of suspicion is needed by physicians evaluating these patients. Overall outcomes are favorable, with recovery to baseline renal function within 3 weeks of discontinuing the offending drug.

Clinical Manifestations and Outcome of Fluoroquinolone Associated Acute Interstitial Nephritis

Abstract Background Fluoroquinolones (FQ) are among the most commonly prescribed antibiotics. Nephrotoxicity related to FQ use is infrequently reported and the mechanism of renal injury is incompletely elucidated. We describe clinical manifestations and outcome of patients with biopsy proven acute interstitial nephritis (AIN) associated with FQ use at our institution. Methods We conducted a retrospective review of biopsy-proven AIN attributed to FQ use at Mayo Clinic Rochester from 1993 to 2016. Cases were reviewed by a renal pathologist and attributed to FQ use by an expert nephrologist. We also reviewed and summarized all published case reports of biopsy proven AIN that were attributed to FQ use. Results We identified 24 patients with FQ-related biopsy-proven AIN. The most commonly used FQ was ciprofloxacin (71%) with median antibiotic treatment duration of 7 days (Figure 1). The median duration between starting FQ and the diagnosis of AIN was 8.5 (IQR: 17). Common clinical manifestations included fever (50%), flank pain (8%), and skin rash (21%). However, 17% of the patients were asymptomatic at the time of diagnosis (Figure 2). Majority (58%) of the patients recovered following discontinuation of antibiotics and returned to baseline renal function at a median of 20.5 (IQR: 15.5). Six patients required temporary hemodialysis and 9 patients received steroids. Conclusion Onset of FQ-related AIN can be delayed and a high index of suspicion is needed by physicians prescribing these agents. Overall outcomes are favorable with recovery to baseline renal function within 3 weeks of discontinuing the offending drug. Disclosures All authors: No reported disclosures.

Cyclooxygenase-2 inhibitor-induced acute interstitial nephritis

A 64-year-old female patient presented to the emergency department with a 3-week history of persistent nausea and vomiting. Her serum creatine prior to admission was 118 µmol/L and on presentation...

Acute interstitial nephritis in the south of Iran; an observational study

Background Acute interstitial nephritis (AIN) is an emerging cause of acute kidney injury (AKI) during the recent years. Objectives: There is no data about prevalence, causes, clinical manifestation and outcomes of AIN in our region. Hence, in this study we aimed to find the prevalence of AIN and describe the causes, clinical presentation, and the outcome of AIN in the native kidney biopsies. Patients and Methods: We reviewed 934 native kidney biopsies from 2006 to 2014 and collected the data of patients with the diagnosis of AIN including medical history, clinical findings, para-clinical data, pathologic findings, treatment and outcomes. Results: Prevalence of AIN in our center during 2006 to 2014 was 2.5% of all renal biopsies. The common cause of AIN in our study was drugs. Of those patients admitted to hospital due to AIN, 17 patients (70.8%) received corticosteroid, five of them (29.4%) received pulse of corticosteroid, and 12 patients (70.6%) received oral drug. Around, 54.2% of the patients had hemodialysis during admission. Eight patients had received both dialysis and corticosteroid. Two of them (8.3%) remained on dialysis and 8 (33.3%) developed chronic kidney disease, but 14 (58.3%) patients recovered. Conclusions: The prevalence of AIN in our study is comparable to other studies and we found the great impact of medications on development of AIN.

Long-term outcome in biopsy-proven acute interstitial nephritis treated with steroids.

Background: There are no prospective randomized controlled trials describing the outcome of acute interstitial nephritis (AIN) treated with steroids, and retrospective studies are limited. Methods: We identified adult patients with a diagnosis of AIN without glomerular pathology over a 14-year period. Treated patients all received oral prednisolone and three also recieved IV methylprednisolone. Data were collected retrospectively on estimated glomerular filtration rate (eGFR), change in eGFR from time of biopsy, dependence on renal replacement therapy (RRT) and mortality, and outcomes were analysed according to the treatment prescribed. Results: A total of 187 eligible patients with AIN were identified and 158 were treated with steroids. There was no difference in median eGFR or dependence on RRT at the time of biopsy. Steroid-treated patients had significantly higher eGFR at all time points post-biopsy up to 24 months, when median eGFR was 43 mL/min in the steroid-treated group and 24 mL/min in the untreated group (P = 0.01). Fewer patients in the steroid-treated group were dialysis dependent by 6 months (3.2% versus 20.6%, P = 0.0022) and 24 months (5.1% versus 24.1%, P = 0.0019). Conclusions: This large retrospective study suggests a benefit of steroids in treatment of AIN with greater improvement in eGFR and fewer patients progressing to end-stage renal disease.

Quiz Page March 2016: A 60-Year-Old Man With Fever, Night Sweats, and Acute Kidney Injury

Quiz Page March 2016: A 60-Year-Old Man With Fever, Night Sweats, and Acute Kidney Injury

The use of gallium-67 scintigraphy in the diagnosis of acute interstitial nephritis.

BackgroundGallium-67 scintigraphy has been suggested as a noninvasive method to diagnose acute interstitial nephritis (AIN). However, its diagnostic performance and usefulness remain controversial.MethodsWe retrospectively reviewed the charts of 76 patients who underwent gallium-67 scintigraphy for a suspicion of AIN. Patients were classified based on kidney biopsy and/or clinical probability of AIN. Gallium-67 scintigraphy results were reinterpreted blindly using both posterior planar and single photon emission computed tomography (SPECT) imaging. Intensity of radioisotope uptake in the kidney was graded from 0 to 5.ResultsThe diagnosis of AIN was confirmed in 23 patients and excluded in 44. Nine patients with an uncertain diagnosis were excluded from subsequent analysis. A gallium-67 kidney uptake cutoff of 1 gave a negative predictive value of 100%, whereas a cutoff of 5 had an excellent specificity and positive predictive value for the diagnosis of AIN. When using a cutoff of 3, which had previously been used in the literature, we obtained a sensitivity of 61% and a specificity of 75% with posterior planar imaging. The results of both SPECT and posterior planar imaging modalities were comparable.ConclusionsGallium-67 scintigraphy may be of interest in patients with a clinical suspicion of AIN, especially in those who are unable to undergo kidney biopsy. However, results need to be interpreted with caution and depend on the intensity of gallium-67 kidney uptake.

A young girl with an unusual cause of acute kidney injury: Answers.

Table ​Table11 lists the differential diagnosis of acute interstitial nephritis (AIN). Table 1 Differential diagnosis of acute interstitial nephritis [9–13]

Tubulointerstitial nephritis and uveitis syndrome in an elderly woman.

Tubulointerstitial nephritis and uveitis syndrome in an elderly woman.

Association of Acute Interstitial Nephritis with Carnivora, a Venus Flytrap Extract, in a 30-Year-Old Man with Hodgkin's Lymphoma.

Acute interstitial nephritis (AIN) is a common cause of acute kidney injury and has been associated with a variety of medications. This is the case of 30-year-old man with Hodgkin's lymphoma who on routine labs before chemotherapy was found to have acute nonoliguric renal failure. A kidney biopsy was performed and confirmed the diagnosis of acute interstitial nephritis. The patient had taken several medications including a higher dose of Carnivora, a Venus flytrap extract, composed of numerous amino acids. The medication was discontinued and kidney function improved towards the patient's baseline indicating that this may be the possible cause of his AIN. Proximal tubular cell uptake of amino acids increasing transcription of nuclear factor-kappaB is a proposed mechanism of AIN from this compound.

Utility of Urine Eosinophils in the Diagnosis of Acute Interstitial Nephritis

Urine eosinophils (UEs) have been shown to correlate with acute interstitial nephritis (AIN) but the four largest series that investigated the test characteristics did not use kidney biopsy as the gold standard. This is a retrospective study of adult patients with biopsy-proven diagnoses and UE tests performed from 1994 to 2011. UEs were tested using Hansel's stain. Both 1% and 5% UE cutoffs were compared. This study identified 566 patients with both a UE test and a native kidney biopsy performed within a week of each other. Of these patients, 322 were men and the mean age was 59 years. There were 467 patients with pyuria, defined as at least one white cell per high-power field. There were 91 patients with AIN (80% was drug induced). A variety of kidney diseases had UEs. Using a 1% UE cutoff, the comparison of all patients with AIN to those with all other diagnoses showed 30.8% sensitivity and 68.2% specificity, giving positive and negative likelihood ratios of 0.97 and 1.01, respectively. Given this study's 16% prevalence of AIN, the positive and negative predictive values were 15.6% and 83.7%, respectively. At the 5% UE cutoff, sensitivity declined, but specificity improved. The presence of pyuria improved the sensitivity somewhat, with a decrease in specificity. UEs were no better at distinguishing AIN from acute tubular necrosis compared with other kidney diseases. UEs were found in a variety of kidney diseases besides AIN. At the commonly used 1% UE cutoff, the test does not shift pretest probability of AIN in any direction. Even at a 5% cutoff, UEs performed poorly in distinguishing AIN from acute tubular necrosis or other kidney diseases.

Cefpodoxime Proxetil-Related Hemolysis and Acute Interstitial Nephritis

We report a case of acute interstitial nephritis (AIN) and immune hemolytic anemia (IHA) associated with cefpodoxime therapy. A patient with a recent history of cefpodoxime proxetil treatment presented with elevated serum creatinine, oliguria, nausea, vomiting, and dyspnea. Evidence of renal failure, abnormal urinalysis, and renal biopsy with inflammatory infiltrate in the interstitium confirmed a diagnosis of AIN. The patient subsequently developed IHA, which was confirmed by peripheral blood smear results and positive Coombs' test. The patient recovered after dialysis therapy and 2 days of intravenous methylprednisolone (500mg/day) followed by oral prednisolone (60 mg/day), which was rapidly tapered and stopped within 3 weeks. To our knowledge, cefpodoxime-induced AIN and IHA are unprecedented. Physicians should be aware that drug-induced AIN and hemolysis can be associated with cefpodoxime proxetil.

Acute kidney injury following isotretinoin treatment

Patient: Female, 17Final Diagnosis: Acute kidney injurySymptoms: Flank pain • nausea • vomitingMedication: IsotretinoinClinical Procedure: Acne treatmentSpecialty: NephrologyObjective: Unknown etiologyBackground:Isotretinoin is widely used for the treatment of acne that is unresponsive to topical therapy. Despite its efficacy, isotretinoin has various adverse effects, including cheilitis, increased risk of cutaneous Staphylococcus aureus infections, and liver function abnormalities.Case Report: A 17-years-old female was admitted to the hospital with a 5-day history of bilateral flank pain, nausea and vomiting. On physical examination, acne was observed over her face treated with Isotretinoin. Both vital signs and physical examination were normal apart from tenderness over both flanks. Initial laboratory results revealed serum creatinine of 2 mg/dl, blood urea nitrogen 20 mg/dl. Complete blood count, full chemistry panel, complements and urinalysis were all normal. Twenty four hours urine collection showed creatinine clearance test of 33 ml/min and urine protein of 390 mg/day. Chest X-ray and ultra sound of kidneys were normal. Acute kidney injury was suspected and she was treated with intravenous fluids. Despite these measures her kidney function steadily worsened. Her serum creatinine on days 2 and 3 were 2.16 and 2.24 mg/dl, respectively. Wright’s staining for eosinophils was positive. Fortunately her serum creatinine started to decrease and was 2 mg/dl and 1.4 mg/dl by day 4 and 5, respectively. A tentative diagnosis of acute interstitial nephritis due to Isotretinoin was made, with the recommendation to avoid this treatment in the future. Two weeks later her serum creatinine and urinary protein returned to normal values.Conclusions:Flank pain should raise suspicion of Isotretinoin-induced acute kidney injury, suggesting that a careful kidney function test besides testing for liver function is warranted in patients with these symptoms.

An Unusual Presentation of Classic Idiopathic Polyarteritis Nodosa as Acute Interstitial Nephritis

In the medical literature, there have been few reported cases of classic Polyarteritis Nodosa (cPAN) presenting with acute renal failure (ARF) and, unlike microscopic polyangiitis (MPA), no documentation to our knowledge of cPAN with clinical presentation similar to acute interstitial nephritis. We describe a case of ARF and a clinical picture suggestive of acute interstitial nephritis (AIN). However, renal biopsy of this patient showed acute necrotizing intrarenal vasculitis, suggestive of cPAN. Although no guidelines exist for the most appropriate therapy for patients presenting in this fashion, combination therapy with cyclophosphamide and steroids, in our patient, resulted in clinical improvement and resolution of dialysis-dependent renal failure. These findings suggest the potential for good prognosis in patients with cPAN who present with a presumed diagnosis of AIN and dialysis-dependent ARF.

Piperacillin–tazobactam-induced acute interstitial nephritis with possible meropenem cross-sensitivity in a patient with osteomyelitis

A 56-year-old man with no known medical history was treated with piperacillin–tazobactam for polymicrobial osteomyelitis and developed acute renal failure with fever and rash after six weeks of therapy. A gallium scan showed mildly increased uptake of radioactive tracer in both kidneys diffusely. A renal ultrasound showed normalsized kidneys without hydronephrosis. Urinalysis revealed eosinophils 5–25% (normal, <1%), hyaline casts, white blood cells, and proteinuria (>1000 mg/dL; normal range, 0–30 mg/dL). He received dialysis and was treated with empirical corticosteroids for acute interstitial nephritis (AIN). The patient’s hospital course was complicated by nosocomial infections requiring treatment with meropenem. After receiving meropenem, the patient developed worsening renal function and a rash that abated after the discontinuation of meropenem, indicating possible cross-sensitivity with piperacillin–tazobactam. AIN can be caused by autoimmune disorders, infections, sarcoidosis, or medications.1,–5 Many drugs (e.g., methicillin, cephalosporins, rifampin, ciprofloxacin, sulfonamides, nonsteroidal antiinflammatory drugs, cimetidine, omeprazole, indinavir) have been reported to cause drug-induced AIN.5,6 Drug-induced AIN is believed to be a hypersensitivity reaction.1 The diagnosis of AIN is usually made by examining the patient’s history, the temporal relation between the onset of AIN and initiation of the offending agent, the presence of certain clinical features and certain laboratory test findings, the exclusion of alternative causes of acute renal failure, a renal biopsy, and an empirical trial with corticosteroids.6

Possible case of nafcillin-induced acute interstitial nephritis

To report a case of acute interstitial nephritis (AIN) secondary to nafcillin. A 55-year-old Hispanic man (height, 63 in.; weight, 61.2 kg) with a history of deep vein thrombosis in the right lower extremity, hypertension, hyperlipidemia, and hepatitis C infection was admitted to the hospital with right-sided chest pain that radiated down his right arm and leg. The patient was diagnosed with methicillin-sensitive Staphylococcus aureus endocarditis. A renal ultrasound was performed on hospital day 9 after the patient developed acute renal failure and showed diffusely increasing echogenicity of the renal parenchymal bilaterally with an interpolar cyst in the left kidney. A urine analysis, serum chemistry panels, and complete blood counts were consistent with AIN. The patient received a total of seven days of nafcillin, and cefazolin was initiated. A renal ultrasound and renal biopsy were performed, which confirmed the diagnosis of AIN. The patient received short-term hemodialysis, after which his renal function slowly returned to baseline. He then underwent an aortic valve replacement and tricuspid valve repair. His antibiotics were changed to rifampin and vancomycin after methicillin-resistant S. aureus was found in an aortic valve culture on hospital day 26. Cefazolin was discontinued 3 days after rifampin and vancomycin were added. The patient received 18 more days of antibiotics and was discharged on the last day of therapy (hospital day 45). A 55-year-old, critically ill man developed a possible case of nafcillin-induced AIN after receiving a 7-day course of treatment with the drug.

Drug-induced acute interstitial nephritis

Acute interstitial nephritis (AIN) is a common cause of acute kidney injury. Many etiologies of AIN have been recognized--including allergic/drug-induced, infectious, autoimmune/systemic, and idiopathic forms of disease. The most common etiology of AIN is drug-induced disease, which is thought to underlie 60-70% of cases. Multiple agents from many different classes of drugs can cause AIN, and the clinical presentation and laboratory findings vary according to the class of drug involved. AIN is characterized by interstitial inflammation, tubulitis, edema, and in some cases, eventual interstitial fibrosis. A definitive diagnosis of AIN can be established only by kidney biopsy. Noninvasive tests such as (67)gallium scintigraphy and testing for eosinophiluria have limited diagnostic utility. The mainstay of therapy for drug-induced AIN is timely discontinuation of the causative agent. Although the benefits of corticosteroid therapy remain unproven, they do appear to have a positive effect in some patients with drug-induced AIN, especially when treatment is initiated early in the course of the disease. In general, the prognosis for drug-induced AIN is good, and at least partial recovery of kidney function is normally observed. Early recognition is crucial because patients can ultimately develop chronic kidney disease.

Characteristics of Patients with HIV and Biopsy-Proven Acute Interstitial Nephritis

The objective of this study was to describe the characteristics of patients with HIV infection and biopsy-proven acute interstitial nephritis (AIN). Pathology reports were reviewed for patients who had HIV infection and underwent renal biopsy at Johns Hopkins Hospital from January 1, 1995, through January 1, 2008. Patients who received a diagnosis of AIN without evidence of HIV-associated nephropathy were identified, and their clinical course was reviewed up to 18 months after biopsy. Of 262 biopsies, 29 (11%) patients who had AIN without evidence of HIV-associated nephropathy were identified. The mean age at the time of biopsy was 47.5 years (range 28 to 71 years), 17 (59%) were men, and 23 (79%) were black. The majority (62%) of patients were on antiretroviral therapy, 59% were current or former intravenous drug users, and 62% had hepatitis C co-infection. Drugs were identified as the cause of AIN in the majority (72%) of cases. Nonsteroidal anti-inflammatory drugs were most commonly implicated, followed by sulfamethoxazole/trimethoprim. Antiretroviral therapy was identified as the cause in only three cases. None of the patients presented with the classic triad of fever, rash, and pyuria, and only seven (24%) patients presented with <1 g/d proteinuria. In our series, AIN was prevalent (11%) and was often drug induced. AIN should not be excluded from the differential diagnosis on the basis of absence of the classic clinical triad of fever, rash, and pyuria.