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Severe preeclampsia is a disorder of pregnancy, characterized by increased blood pressure (>140/90 mmHg) and proteinuria (≥ 300 mg/24 hours) at later than 20 weeks of gestation. Particularly in underdeveloped nations, severe preeclampsia and eclampsia have a significant negative impact on the health of expectant mothers, fetuses, and newborns. The HELLP (hemolysis, increased liver enzymes, low platelets) syndrome is thought to be a subset of preeclampsia, a group of hypertensive disorders of pregnancy that also includes eclampsia. Compared to preeclampsia alone, maternal and fetal problems are more severe in HELLP. There can be a diagnostic dilemma that arises when attempting to differentiate HELLP from its numerous imitators to determine the appropriate course of treatment. Here, we present a rare case of a pregnant woman presenting with preeclampsia complicated by manifestations and investigations suggestive of HELLP syndrome with acute kidney injury (AKI), retinal detachment, and symptoms of DIC (disseminated intravascular coagulation), which can be grievous to the mother as well as the fetus.
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We present a case of lamotrigine-triggered DRESS (drug reaction with eosinophilia and systemic symptoms) syndrome with acute kidney injury stage 3. A 17-year-old girl with known epilepsy treated with lamotrigine presented with acute kidney injury as well as skin eruption, fever, and apathy. Extended diagnostics, considering infectious and autoimmune diseases, remained unremarkable. Lamotrigine blood levels were within the target range. Kidney biopsy showed acute interstitial nephritis with tubular necrosis. Methylprednisolone pulse therapy led to an improvement in kidney function; skin eruption and neurological symptoms resolved. During the hospital stay, the girl admitted to inconsistent and variable intake of lamotrigine, occasionally resulting in notable overdosing. This report demonstrates that acute kidney injury in lamotrigine-induced DRESS syndrome is an acute interstitial nephritis with tubular necrosis, an aspect that has not been deeply characterized so far. Additionally, we aim to elevate awareness towards non-adherence as cause of disease, especially among the adolescent population.
Asunto(s)
Lesión Renal Aguda , Anticonvulsivantes , Síndrome de Hipersensibilidad a Medicamentos , Lamotrigina , Triazinas , Humanos , Lamotrigina/efectos adversos , Lamotrigina/uso terapéutico , Femenino , Adolescente , Síndrome de Hipersensibilidad a Medicamentos/etiología , Síndrome de Hipersensibilidad a Medicamentos/diagnóstico , Síndrome de Hipersensibilidad a Medicamentos/tratamiento farmacológico , Lesión Renal Aguda/inducido químicamente , Lesión Renal Aguda/diagnóstico , Triazinas/efectos adversos , Anticonvulsivantes/efectos adversos , Metilprednisolona/uso terapéutico , Metilprednisolona/administración & dosificación , Epilepsia/tratamiento farmacológico , Nefritis Intersticial/inducido químicamente , Nefritis Intersticial/diagnóstico , BiopsiaRESUMEN
Acute kidney injury (AKI) involves a rapid decline in kidney function, classified into prerenal, intrarenal, and postrenal causes. Drug-induced AKI's complex pathophysiology includes altered hemodynamics, inflammation, crystal deposition, hemolysis, and rhabdomyolysis. This report details a 42-year-old female with hypertension and diabetes who, following a dog bite, exhibited reduced kidney function (GFR: 16 ââmL/min/1.73m2; BUN/Cr: 23/3.23 mg/dL). A renal ultrasound revealed no stones or masses, and the recent use of tirzepatide was identified. Discontinuation of the drug, IV fluid maintenance, and close monitoring led to swift kidney function improvement. This case underscores the importance of recognizing drug-induced AKI, even in unrelated complaints, and highlights the need for vigilance and research into the adverse effects of medications such as glucagon-like peptide 1 (GLP-1) receptor agonists.
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Nephrotoxicity is one of the most important complications in cancer patients. In particular, acute kidney injury (AKI) is known to be associated with discontinuing effective oncological treatments, longer hospitalizations, increased costs, and a higher risk of death. In addition to acute kidney injury, clinical signs associated with nephrotoxicity during treatment with anticancer agents include chronic kidney disease, proteinuria, hypertension, electrolyte abnormalities, and other characteristic manifestations. Many of these signs are caused both by cancer treatment as well as by cancer itself. Therefore, it is important to carefully recognize whether the underlying causes of renal impairment in cancer patients are cancer-related, treatment-related, or both. This review describes the epidemiology and pathophysiology of anticancer agent-induced acute kidney injury, proteinuria, hypertension, and other characteristic manifestations.
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Lesión Renal Aguda , Antineoplásicos , Hipertensión , Neoplasias , Humanos , Nefrólogos , Antineoplásicos/efectos adversos , Lesión Renal Aguda/inducido químicamente , Lesión Renal Aguda/epidemiología , Proteinuria/inducido químicamente , Neoplasias/tratamiento farmacológico , Neoplasias/complicacionesRESUMEN
The prognosis of sarcomatoid renal cell carcinoma has changed dramatically with the emergence of immune checkpoint inhibitors. Notably the use of nivolumab and ipilimumab combination therapy has demonstrated promising durable therapeutic response for patients with treatment-naïve sarcomatoid renal-cell carcinoma. We present a case of 45-year-old man with a history of metastatic sarcomatoid renal cell carcinoma treated with nivolumab plus ipilimumab who developed type 1 diabetes mellitus, adrenal insufficiency, thyroiditis/hypothyroidism, and acute interstitial nephritis as a result of immunotherapy.
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Carcinoma de Células Renales , Neoplasias Renales , Nefritis Intersticial , Protocolos de Quimioterapia Combinada Antineoplásica/efectos adversos , Humanos , Ipilimumab/efectos adversos , Masculino , Persona de Mediana Edad , Nefritis Intersticial/inducido químicamente , Nefritis Intersticial/diagnóstico , Nivolumab/uso terapéuticoRESUMEN
Bird death is often caused by renal lesions induced by chemicals. The avian kidney has a renal portal system with significant blood flow that is sensitive to many chemicals. However, early avian biomarkers for kidney injury are yet to be identified. This study aimed to identify novel renal biomarkers. Acute kidney injury (AKI) can be divided into acute interstitial nephritis (AIN) and acute tubular necrosis (ATN). A chicken model of kidney damage was created by an injection of diclofenac or cisplatin, which caused either AIN or ATN, respectively. Microarray analysis was performed to profile the gene expression patterns in the chickens with nephropathy. A gene enrichment analysis suggested that the genes related to responses to external stimuli showed expression changes in both AIN and ATN. However, hierarchical clustering analyses suggested that gene expression patterns differed between AIN and ATN, and the number of biomarkers relating to renal damage was low. To identify early biomarkers for nephropathy, we focused on genes that were induced at various levels of renal damage. The gene, vanin-1 (VNN1) was highly induced in the early stages of renal damage. A quantitative real-time PCR analysis supported this finding. These results suggest VNN1 could be a useful early biomarker of kidney injury in avian species.
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Necrosis Tubular Aguda , Nefritis Intersticial , Animales , Biomarcadores/metabolismo , Pollos/genética , Pollos/metabolismo , Perfilación de la Expresión Génica/veterinaria , Riñón/metabolismo , Necrosis Tubular Aguda/metabolismo , Necrosis Tubular Aguda/patología , Necrosis Tubular Aguda/veterinaria , Nefritis Intersticial/metabolismo , Nefritis Intersticial/patología , Nefritis Intersticial/veterinariaRESUMEN
INTRODUCTION: Acute kidney injury (AKI) is a worldwide concern and it leads to a poor prognosis or end-stage kidney disease. The purpose of this study was to clarify the characteristics of patients with AKI in whom kidney biopsy was performed using data of the Japan Renal Biopsy Registry (J-RBR). METHODS: We screened 38,351 cases that were registered in the J-RBR from 2007 to 2018. We obtained data for 383 patients with AKI based on clinical diagnosis for analysis 1 and data for 714 patients with acute interstitial nephritis (AIN) or acute tubular necrosis (ATN) based on pathological diagnosis for analysis 2. RESULTS: Of the cases screened, 383 patients with AKI (1.0%) were included in analysis 1. The main pathological diagnoses of AKI were AIN, ATN, chronic interstitial nephritis, nephro-sclerosis and crescentic glomerulonephritis. Of the cases screened, 589 patients with AIN (1.5%) and 110 patients with ATN (0.3%) were included in analysis 2. The main clinical diagnoses of AIN were AKI, rapidly progressive glomerulonephritis (RPGN), chronic nephritic syndrome (CNS) and drug-induced nephropathy (DIN), whereas those of ATN were AKI, RPGN, DIN and CNS. ATN patients had a higher serum creatinine level than that of AIN patients. CONCLUSION: Our results revealed that cases in the J-RBR included 1.0% of AKI cases based on clinical diagnosis and 1.5% and 0.3% of AIN and ATN cases, respectively, based on pathological diagnosis. In patients with suspected intrinsic AKI, kidney biopsy should be performed for diagnosis of the precise etiology and selection of appropriate treatment.
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Lesión Renal Aguda , Glomerulonefritis , Nefritis Intersticial , Nefritis , Lesión Renal Aguda/terapia , Biopsia , Creatinina , Estudios Transversales , Glomerulonefritis/patología , Hematuria/patología , Humanos , Japón/epidemiología , Riñón/patología , Nefritis/patología , Nefritis Intersticial/diagnóstico , Nefritis Intersticial/patología , Pronóstico , Proteinuria/patología , Sistema de RegistrosRESUMEN
Chikungunya nephropathy is an uncommon etiology of acute kidney injury, associated with the mosquito-borne chikungunya arbovirus (CHIKV). The very limited number of pathologic reports to date have only involved postmortem analyses. We here report 5 cases of acute kidney injury for which kidney biopsies were performed in patients with confirmed acute CHIKV infection, during the recent outbreak of chikungunya disease in the French West Indies. The patients ranged from 42 to 76 years of age. All of the patients developed kidney injury, 3 of whom required short-term dialysis and underwent a kidney biopsy. Analysis of kidney biopsies revealed 2 main histopathologic patterns: acute interstitial nephritis with predominant lymphoid inflammation and acute tubular injury. Epithelioid granulomas were observed in 2 cases. There were no glomerular lesions, except in biopsies from 2 patients, including 1 with a previous known primary focal segmental glomerulosclerosis. CHIKV antigen immunofluorescence microscopy revealed staining in tubular cells. In all of the cases, the short-term outcome was favorable, with recovery of kidney function.
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Lesión Renal Aguda , Fiebre Chikungunya , Nefritis Intersticial , Lesión Renal Aguda/diagnóstico , Lesión Renal Aguda/epidemiología , Lesión Renal Aguda/etiología , Animales , Biopsia , Fiebre Chikungunya/complicaciones , Fiebre Chikungunya/diagnóstico , Fiebre Chikungunya/epidemiología , Humanos , RiñónRESUMEN
For over 70 years, serum creatinine has remained the primary index for detection and monitoring of kidney disease. Tubulointerstitial damage and fibrosis are highly prognostic for subsequent kidney failure in biopsy studies, yet this pathology is invisible to the clinician in the absence of a biopsy. Recent discovery of biomarkers that reflect distinct aspects of kidney tubule disease have led to investigations of whether these markers can provide additional information on risk of chronic kidney disease (CKD) progression and associated adverse clinical end points, above and beyond estimated glomerular filtration rate and albuminuria. These biomarkers can be loosely grouped into those that mark tubule cell injury (eg, kidney injury molecule 1, monocyte chemoattractant protein 1) and those that mark tubule cell dysfunction (eg, α1-microglobulin, uromodulin). These kidney tubule biomarkers provide new opportunities to monitor response to therapeutics used to treat CKD patients. In this review, we describe results from some unique contributions in this area and discuss the current challenges and requirements in the field to bring these markers to clinical practice. We advocate for a broader assessment of kidney health that moves beyond a focus on the glomerulus, and we highlight how such tools can improve diagnostic accuracy and earlier assessment of therapeutic efficacy or harm in CKD patients.
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Insuficiencia Renal Crónica , Albuminuria , Biomarcadores , Tasa de Filtración Glomerular , Humanos , Túbulos Renales , Insuficiencia Renal Crónica/diagnósticoRESUMEN
Proton pump inhibitors (PPIs), long thought to be safe, are associated with a number of nonkidney adverse health outcomes and several untoward kidney outcomes, including hypomagnesemia, acute kidney injury, acute interstitial nephritis, incident chronic kidney disease, kidney disease progression, kidney failure, and increased risk for all-cause mortality and mortality due to chronic kidney disease. PPIs are abundantly prescribed, rarely deprescribed, and frequently purchased over the counter. They are frequently used without medical indication, and when medically indicated, they are often used for much longer than needed. In this In Practice review, we summarize evidence linking PPI use with adverse events in general and adverse kidney outcomes in particular. We review the literature on the association of PPI use and risk for hypomagnesemia, acute kidney injury, acute interstitial nephritis, incident chronic kidney disease, kidney disease progression, end-stage kidney disease, and death. We provide an assessment of how this evidence should inform clinical practice. We review the impact of this evidence on patients' perception of risk, synthesize PPI deprescription literature, and provide our recommendations on how to approach PPI use and deprescription.
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Deprescripciones , Medicina Basada en la Evidencia/métodos , Enfermedades Renales/inducido químicamente , Enfermedades Renales/prevención & control , Inhibidores de la Bomba de Protones/efectos adversos , Prescripciones de Medicamentos/normas , Medicina Basada en la Evidencia/normas , Humanos , Enfermedades Renales/diagnóstico , Factores de RiesgoRESUMEN
Tick-borne illnesses are a growing problem in the United States. Human granulocytic anaplasmosis (HGA), carried by the Ixodes scapularis tick, is caused by Anaplasma phagocytophilum. While the clinical manifestations of HGA may be protean, ranging from asymptomatic infection to life-threatening multiorgan failure, renal involvement is uncommon. We report a case of a 64-year-old man presenting with a febrile illness and acute nephritis in the setting of HGA infection. The patient's kidney biopsy was characterized by a membranoproliferative glomerulonephritis pattern and acute interstitial inflammation. After appropriate antibiotic treatment and high-dose steroids, the patient had a marked improvement in kidney function, although a subsequent recrudescence of nephritis required a 6-month course of additional steroids. As the prevalence of tick-borne diseases continues to spread across the United States, raising awareness of the potential for atypical presentations is important, particularly because early diagnosis and treatment can be curative and prevent further complications.
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Lesión Renal Aguda/etiología , Anaplasmosis/complicaciones , Glucocorticoides/administración & dosificación , Riñón/patología , Lesión Renal Aguda/diagnóstico , Lesión Renal Aguda/tratamiento farmacológico , Anaplasma phagocytophilum/aislamiento & purificación , Anaplasmosis/diagnóstico , Anaplasmosis/tratamiento farmacológico , Antibacterianos/uso terapéutico , Relación Dosis-Respuesta a Droga , Quimioterapia Combinada , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Immune checkpoint inhibitors are increasingly used to treat a variety of solid-organ and hematologic cancers. However, overactivation of the immune system can lead to immune-related adverse events, which are increasingly recognized in the kidney. There have been only rare reported cases of checkpoint inhibitor-associated glomerulonephritis and renal vasculitis, although vasculitis in other organs has been well described. We report 4 cases of renal vasculitis or pauci-immune glomerulonephritis after checkpoint inhibitor therapy. Three patients had renal small- to medium-vessel vasculitis and 1 had focally crescentic pauci-immune glomerulonephritis. Three patients presented with acute kidney injury, and 1 presented with nephrotic syndrome and hematuria. Three patients were tested for antineutrophil cytoplasmic antibodies, which were negative. The time from checkpoint inhibitor initiation to immune-related adverse event presentation ranged from 2 weeks to 24 months. Three patients were treated with glucocorticoids, resulting in clinical resolution. Our series demonstrates that renal vasculitis and pauci-immune glomerulonephritis are important considerations in the differential diagnosis of checkpoint inhibitor-related reductions in kidney function.
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Lesión Renal Aguda/inducido químicamente , Anticuerpos Monoclonales Humanizados/efectos adversos , Antineoplásicos Inmunológicos/efectos adversos , Glomerulonefritis Membranosa/inducido químicamente , Nivolumab/efectos adversos , Lesión Renal Aguda/patología , Adenocarcinoma/tratamiento farmacológico , Adenocarcinoma/patología , Anciano , Anticuerpos Monoclonales Humanizados/uso terapéutico , Antineoplásicos Inmunológicos/uso terapéutico , Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Carcinoma de Pulmón de Células no Pequeñas/patología , Femenino , Estudios de Seguimiento , Glomerulonefritis Membranosa/patología , Humanos , Neoplasias Pulmonares/tratamiento farmacológico , Neoplasias Pulmonares/patología , Masculino , Melanoma/tratamiento farmacológico , Melanoma/patología , Persona de Mediana Edad , Nivolumab/uso terapéutico , Neoplasias del Recto/tratamiento farmacológico , Neoplasias del Recto/patología , Medición de Riesgo , Muestreo , Tasa de SupervivenciaRESUMEN
Automated urine technology and centralized laboratory testing are becoming the standard for providing urinalysis data to clinicians, including nephrologists. This trend has had the unintended consequence of making examination of urine sediment by nephrologists a relatively rare event. In addition, the nephrology community appears to have lost interest in and forgotten the utility of provider-performed urine microscopy. However, it is critical to remember that urine sediment examination remains a time-honored test that provides a wealth of information about the patient's underlying kidney disease. This test performs very favorably as a urinary "biomarker" for a number of acute kidney diseases. When used properly, urine sediment findings alert health care providers to the presence of kidney disease, while also providing diagnostic information that often identifies the compartment of kidney injury. Urine sediment findings may also guide therapy and assist in prognostication. In this review of the role of urine sediment examination in the diagnosis and management of kidney disease, we seek to help experienced nephrologists maintain their competency in performing this test and encourage ongoing training of nephrology fellows and others less experienced in such analyses.
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Curriculum , Enfermedades Renales/terapia , Enfermedades Renales/orina , Nefrólogos/educación , Urinálisis/métodos , Lesión Renal Aguda/diagnóstico , Lesión Renal Aguda/terapia , Lesión Renal Aguda/orina , Biomarcadores/orina , Manejo de la Enfermedad , Femenino , Humanos , Enfermedades Renales/diagnóstico , Masculino , Microscopía/métodos , Nefrología/educaciónRESUMEN
Vedolizumab is a gut-selective humanized monoclonal antibody that binds selectively to the α4 ß7 integrin and acts as a lymphocyte-homing antagonist. It is indicated in ulcerative colitis and Crohn disease. We report a case of acute interstitial nephritis following vedolizumab infusion in a 55-year-old white woman treated for severe Crohn disease resistant to several therapies. Other kidney disease causes were ruled out. Glucocorticoids were administrated, leading to full renal recovery. In the absence of other therapeutic options, vedolizumab was re-administered along with transient corticosteroids; this treatment was well tolerated. Fewer than 10 cases of immunoallergic acute interstitial nephritis following treatment with monoclonal antibody have previously been reported in the literature. The pathophysiology of delayed-type hypersensitivity secondary to monoclonal antibody therapeutics is discussed in this case report.
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Anticuerpos Monoclonales Humanizados , Enfermedad de Crohn , Glucocorticoides/administración & dosificación , Pruebas de Función Renal/métodos , Nefritis Intersticial , Anticuerpos Monoclonales Humanizados/administración & dosificación , Anticuerpos Monoclonales Humanizados/efectos adversos , Enfermedad de Crohn/tratamiento farmacológico , Enfermedad de Crohn/metabolismo , Hipersensibilidad a las Drogas , Femenino , Fármacos Gastrointestinales/administración & dosificación , Fármacos Gastrointestinales/efectos adversos , Humanos , Infusiones Intravenosas , Integrinas/antagonistas & inhibidores , Persona de Mediana Edad , Nefritis Intersticial/inducido químicamente , Nefritis Intersticial/diagnóstico , Nefritis Intersticial/inmunología , Nefritis Intersticial/terapia , Recuperación de la Función , Resultado del TratamientoRESUMEN
Immune checkpoint inhibitors that target the programmed death 1 (PD-1) signaling pathway have recently been approved for use in advanced pretreated non-small cell lung cancer and melanoma. Clinical trial data suggest that these drugs may have adverse effects on the kidney, but these effects have not been well described. We present 6 cases of acute kidney injury in patients with lung cancer who received anti-PD-1 antibodies, with each case displaying evidence of acute interstitial nephritis (AIN) on kidney biopsy. All patients were also treated with other drugs (proton pump inhibitors and nonsteroidal anti-inflammatory drugs) linked to AIN, but in most cases, use of these drugs long preceded PD-1 inhibitor therapy. The association of AIN with these drugs in our patients raises the possibility that PD-1 inhibitor therapy may release suppression of T-cell immunity that normally permits renal tolerance of drugs known to be associated with AIN.
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Anticuerpos Monoclonales Humanizados/efectos adversos , Anticuerpos Monoclonales/efectos adversos , Antineoplásicos/efectos adversos , Carcinoma de Pulmón de Células no Pequeñas/tratamiento farmacológico , Neoplasias Pulmonares/tratamiento farmacológico , Nefritis Intersticial/inducido químicamente , Enfermedad Aguda , Anciano , Anticuerpos Monoclonales/uso terapéutico , Anticuerpos Monoclonales Humanizados/uso terapéutico , Antineoplásicos/uso terapéutico , Proteínas Reguladoras de la Apoptosis/antagonistas & inhibidores , Muerte Celular/efectos de los fármacos , Femenino , Humanos , Masculino , Persona de Mediana Edad , NivolumabRESUMEN
BACKGROUND: Acute interstitial nephritis (AIN) is an important cause of acute kidney injury, especially in hospitalized patients. The cause and outcome of AIN, particularly that due to drugs, is changing with prevalent medication use. The effectiveness of steroids for treatment of AIN is debated. STUDY DESIGN: Case series. SETTING & PARTICIPANTS: 133 patients with biopsy-proven AIN from 1993 through 2011 at a single center. OUTCOMES: Recovery of kidney function by 6 months, either complete, partial, or none. Complete recovery was defined as improvement in serum creatinine level to within 25% of baseline (or < 1.4 mg/dL), and partial recovery, as a ≥ 50% decrease in serum creatinine level from its peak value but not reaching within 25% of its baseline value. RESULTS: Causes of AIN included drugs (70%), autoimmune diseases (20%), and infections (4%). Drug-induced AIN was due to antibiotics in 49%, proton pump inhibitors (PPIs) in 14%, and nonsteroidal anti-inflammatory drugs (NSAIDs) in 11%. Overall, the top 3 drug causes were omeprazole (12%), amoxicillin (8%), and ciprofloxacin (8%). Patients with drug-induced compared to non-drug-induced AIN were older and had higher baseline kidney function, but more severe acute kidney injury. Patients with PPI-induced AIN were older, were less symptomatic, and had longer durations of drug exposure and longer delays in getting kidney biopsy and steroids than for antibiotic-induced or NSAID-induced AIN. At 6 months postbiopsy, 49% of patients with drug-induced AIN treated with steroids achieved complete recovery; 39%, partial recovery; and 12%, no recovery. Correlates of poor recovery included a longer duration of drug exposure (15 vs 30 vs 130 days for complete, partial, and no recovery, respectively; P = 0.04) and longer delay in starting steroid therapy (8 vs 11 vs 35 days, respectively; P = 0.05). LIMITATIONS: Retrospective study, selection bias in patients who had kidney biopsy, single-center experience. CONCLUSIONS: The cause of AIN may be shifting; PPIs are emerging as an important contributor to this disease. Delays in discontinuation of the culprit drug and in initiating steroid treatment adversely affect recovery of kidney function.