Non-oliguric Acute Kidney Injury Research Articles

#3033 IgA vasculitis: a unexpected diagnosis of pulmonary renal syndrome

Abstract Background IgA vasculitis is an inflammatory condition affecting blood vessels that poses a significant diagnostic and therapeutic challenge in clinical practice. Characterized by the deposition of immunoglobulin A (IgA) on vessel walls, this pathology can manifest in various ways, presenting a broad and sometimes complex clinical spectrum. Ninety percent of cases occur in the pediatric age group. Severe lung involvement, such as pulmonary hemorrhage, is rare in patients with IgAV. We present a case of a 33-year-old patient with pulmonary renal syndrome and without purpura, an atypical presentation of IgA vasculitis. Case Report We describe the case of a 33-year-old patient with no relevant medical history or regular medication, who presented to the emergency department in November 2022 with symptoms of hemoptysis, fatigue, myalgias, and pallor. On physical examination, the patient was conscious, cooperative, normotensive, tachycardic, afebrile, with bilateral axillary adenopathies, and scattered crackles on lung auscultation. Laboratory tests revealed anemia with a hemoglobin level of 5.8 g/dL, non-oliguric acute kidney injury with a creatinine level of 2.25 mg/dL, microscopic hematuria (>50/hpf), and proteinuria (UPCR of 2.8 mg/mg and UACR of 1.6 mg/mg). A chest CT scan showed bilateral and scattered ground-glass opacities consistent with alveolar hemorrhage. The patient was admitted to the Nephrology service, underwent 3 sessions of plasma exchange, and started therapy with methylprednisolone 1000 mg for 3 days. A renal biopsy revealed 24 glomeruli, with 3 showing segmental sclerosis and 1 with fibrocellular crescents, mild interstitial nephritis; immunofluorescence showed IgA+++, C3++, IgM, and IgG+- Oxford Classification: M1 E0 S1 T0 C1. Bronchofibroscopy showed a rosy bronchoalveolar lavage and macrophages with hemosiderin pigment deposition. The patient continued with prednisolone at 1 mg/kg. In January 2023 (after two months), there was a >25% reduction in albuminuria with resolution of acute kidney injury. A gradual reduction of prednisolone was initiated, and it was definitively discontinued in October 2023. In the last outpatient visit in January 2024, the patient maintained normal renal function, with no hematuria, UPCR of 100 mg/g, UACR of 70 mg/g, and no further episodes of alveolar hemorrhage. Conclusion This case stands out for its atypical presentation: an adult with alveolar hemorrhage and without other more classical manifestations of IgA vasculitis, such as purpura. This is yet another case that emphasizes the importance of the broad spectrum of diagnoses that a nephrologist should consider in the face of acute kidney injury.

Endothelium-related biomarkers enhanced prediction of kidney support therapy in critically ill patients with non-oliguric acute kidney injury

Acute kidney injury (AKI) is a common condition in hospitalized patients who often requires kidney support therapy (KST). However, predicting the need for KST in critically ill patients remains challenging. This study aimed to analyze endothelium-related biomarkers as predictors of KST need in critically ill patients with stage 2 AKI. A prospective observational study was conducted on 127 adult ICU patients with stage 2 AKI by serum creatinine only. Endothelium-related biomarkers, including vascular cell adhesion protein-1 (VCAM-1), angiopoietin (AGPT) 1 and 2, and syndecan-1, were measured. Clinical parameters and outcomes were recorded. Logistic regression models, receiver operating characteristic (ROC) curves, continuous net reclassification improvement (NRI) and integrated discrimination improvement (IDI) were used for analysis. Among the patients, 22 (17.2%) required KST within 72 h. AGPT2 and syndecan-1 levels were significantly greater in patients who progressed to the KST. Multivariate analysis revealed that AGPT2 and syndecan-1 were independently associated with the need for KST. The area under the ROC curve (AUC-ROC) for AGPT2 and syndecan-1 performed better than did the constructed clinical model in predicting KST. The combination of AGPT2 and syndecan-1 improved the discrimination capacity of predicting KST beyond that of the clinical model alone. Additionally, this combination improved the classification accuracy of the NRI and IDI. AGPT2 and syndecan-1 demonstrated predictive value for the need for KST in critically ill patients with stage 2 AKI. The combination of AGPT2 and syndecan-1 alone enhanced the predictive capacity of predicting KST beyond clinical variables alone. These findings may contribute to the early identification of patients who will benefit from KST and aid in the management of AKI in critically ill patients.

Profile of Acute Kidney Injury in the Pediatric Age Group in a Tertiary Care Hospital: A Prospective Observational Study.

Acute kidney injury (AKI) is a menace in the pediatric intensive care unit (PICU) and is responsible for significant morbidity and mortality all over the world. There are limited data available on pediatric AKI in central India. Our primary objective is to determine the clinical, etiological, and outcome profile of AKI in the pediatric age group of 3 months to 15 years admitted to the All India Institute of Medical Sciences (AIIMS), Raipur. The secondary objective(s) is to predict the association of mortality in children diagnosed with AKI and to estimate the number of patients developing chronic kidney disease (CKD) at three-month follow-up. This observational study was conducted in the Department of Pediatrics at AIIMS Raipur, Chhattisgarh, from September 2021 to February 2023. All patients aged 3 months to 15 years of age satisfying the Kidney Disease: Improving Global Outcomes (KDIGO) criteria for AKI and presenting to the hospital were included, and those refusing consent or having CKD stage ≥3 were excluded. A total of 66 children were assessed for eligibility. Out of these 66 patients, 2 were excluded as they had AKI on CKD, and a total of 64 patients were included. For all included patients, details of their demography, clinical features, etiology workup, and hospital stay were collected. Their outcome was observed and categorized into complete response, partial response, no response, left against medical advice (LAMA), or death. Patients who were discharged were followed up for three months and observed for the recovery or development of CKD. The incidence of AKI in the PICU was 15.48% (64/413). Ventricular septal defect with pneumonia and pneumonia (12.5%, 8/64 each) were the most common diagnoses at presentation, resulting in AKI. The most common clinical presentations were fever (54.7%, 35/64) and respiratory distress (43.8%, 28/64). Out of them, 73.4% (47/64) had sepsis, and 62.5% (40/64) had shock. About 56.2% (36/64) of children had non-oliguric AKI as compared to 43.8% (28/64) who had oliguric AKI. Among total children with AKI, 54.7% (35/64) of patients had prerenal AKI, 43.8% (28/64) had renal AKI, and 1.6% (1/64) had postrenal AKI. Of all the children included, 32.8% (21/64) experienced complete resolution of AKI, while 18.8% (12/64) showed partial resolution, and 1.6% (1/64) remained unresolved. Among them, 3.1% (2/64) LAMA, and 43.8% (28/64) died. The median duration of the hospital stay in our study was 16.5 days. Out of them, 59.4% (38/64) of patients required renal replacement therapy (60.5% required peritoneal dialysis (PD), 36.8% required hemodialysis (HD), and 2.6% required both). Among survivors, 19.35% (6/31) developed CKD on a three-month follow-up. The incidence of AKI was seen in critically ill children in the PICU, and it was associated with high mortality.

Nutritional management of sepsis secondary to infective acute gastroenteritis with diabetes

ABSTRACT A 36-year-old Chinese male was presented at the emergency department and admitted to the Geriatric Intensive Care Unit for severe diabetic ketoacidosis (DKA) secondary to acute gastroenteritis (AGE) with symptoms of severe vomiting and diarrhoea. He had underlying maturity-onset diabetes of the young, hypertension, dihydrolipoamide dehydrogenase dihydrolipoamide dehydrogenase (DLD) and chronic kidney disease Stage 3 and had a history of hospital admission for the episodes of hypoglycaemia. The current diagnosis was sepsis secondary to infective AGE, resolved DKA, non-oliguric acute kidney injury, neck haematoma and left-hand cellulitis. He was referred to dietitian for diabetic counselling. His calculated body mass index was 19.4 kg/m2 (normal) with no history of fat and muscle loss. The biochemical data showed abnormalities for glycated haemoglobin, renal profile, liver function test and full blood count.

Predictors of oliguria in post-traumatic acute kidney injury

BackgroundAcute kidney injury is classified by urine output into non-oliguric and oliguric variants. Non-oliguric acute kidney injury has lower morbidity and mortality and accounts for up to 64% of acute kidney injury in hospitalized patients. However, the incidence of non-oliguric acute kidney injury in the trauma population and whether the 2 variants of acute kidney injury share the same risk factors is unknown. We hypothesized that oliguria would be present in the majority of acute kidney injury in severely injured trauma patients and that unique risk factors would predispose patients to the development of oliguria. MethodsPatients admitted to the trauma intensive care unit and diagnosed with an acute kidney injury between 2016 to 2021 were identified. Cases were categorized based on urine output into oliguric (<400 mL per day) and non-oliguric (>400 mL per day) disease. Risk factors, management, and outcomes were compared. Logistic regression was used to identify risk factors associated with oliguria. ResultsA total of 227 patients met inclusion criteria. Non-oliguric acute kidney injury accounted for 74% of all cases and was associated with greater survival (78% vs 35.6%, P < .001). Using logistic regression, female sex, vasopressor use, and a greater net fluid balance at 48 hours were all predictive of oliguria (while controlling for age, race, shock index, massive transfusion, operative intervention, cardiac arrest, and nephrotoxic medication exposure). ConclusionNon-oliguria accounts for the majority of post-traumatic acute kidney injury and is associated with improved survival. Specific risk factors for the development of oliguric acute kidney injury include female sex, vasopressor use, and a higher net fluid balance at 48 hours.

Tubular Interstitial Nephritis Secondary to Herbal Consumption: Case Report and Literature Review

Acute tubular interstitial nephritis is a form of immune-mediated renal injury characterized by infiltration of immune cells in the renal tubulointerstitium, leading to oliguric or non-oliguric acute kidney injury. It manifests with systemic arterial hypertension, foamy urine, and sometimes with secondary anemia if there is progression to chronic renal disease. The diagnosis of certainty is made by biopsy, the initial treatment consists of identifying and removing the triggering agent to avoid further exposure to toxins, management of the acute renal lesion and in some cases, it may be decided to start corticosteroids to avoid progression to end-stage chronic kidney disease. We present the case of a 24-year-old female patient with a history of consumption of unspecified herbal medicine for aesthetic purposes 3 years prior to our evaluation, who debuted with hypertensive emergency manifested by hypertensive retinopathy, hypertensive renal vasculopathy and tubulointerstitial nephritis, successfully treated with the withdrawal of the aggressor agent, angiotensin converting enzyme inhibitors, nitrates and corticosteroids. After 6 months of follow-up, the patient is asymptomatic and with total recovery of the renal disease documented by normal creatinine in laboratory tests.

Incidence, Risk Factors, and Outcomes of Acute Kidney Injury in Preterm Neonates Hospitalized in the Neonatology Unit, North India: A Single-center Experience.

Acute kidney injury (AKI) is common in premature newborns and is associated with high mortality. It is unclear which risk factors lead to AKI in these neonates. We aimed to determine the incidence, risk factors, and outcomes of AKI in preterm neonates in the neonatal intensive care unit (NICU). They were screened and staged for AKI as per the amended neonatal criteria of Kidney Disease Improving Global Outcomes and followed up until discharge or death. Serum creatinine levels and urine output were measured. The incidence of AKI was 18.5% (37/200 neonates). The majority developed non-oliguric AKI. The risk factors significantly associated with AKI in neonates were the presence of sepsis, birth asphyxia, shock, respiratory distress syndrome, and hypothermia. The majority of neonates with AKI had a birthweight <1500 g and a gestational age of <32 weeks and had a higher risk of mortality, in contrast to than those without AKI. Mortality and NICU stay were significantly higher among those with Stage 3 AKI compared with Stage 2 and Stage 1 AKI. To prevent AKI and reduce the burden of high mortality in premature neonates, it is essential to prevent sepsis, birth asphyxia, and respiratory distress syndrome, as well as to detect shock and patent ductus arteriosus as early as possible. There is a need for good antenatal care to reduce the burden of prematurity.

Neurodevelopment After Neonatal Acute Kidney Injury in Very Preterm-Birth Children

This study aimed to assess head circumference (HC) growth and neurodevelopmental outcomes in very preterm-birth children after neonatal acute kidney injury (AKI). This longitudinal follow-up cohort included 732 very preterm neonates of gestational age<31 weeks admitted to a tertiary center between 2008 and 2020. AKI was categorized as nonoliguric and oliguric AKI based on the urine output criteria during admission. We compared the differences in death, z scores of HC (zHC) at term-equivalent age (TEA) and at corrected ages of 6, 12, and 24 months, and the neurodevelopmental outcomes at corrected age of 24 months after neonatal nonoliguric and oliguric AKI. Among the 154 neonates who developed AKI, 72 had oliguric AKI and 82 had nonoliguric AKI. At TEA, oliguric AKI, but not nonoliguric AKI, was independently associated with lower zHC than non-AKI (mean differences,-0.49; 95% confidence interval [CI],-0.92 to-0.06). Although the 3 groups were comparable in zHC at corrected ages of 6, 12, and 24 months, the oliguric AKI group, but not the nonoliguric AKI group, had a higher rate of microcephaly by corrected age of 24 months. In addition, the oliguric AKI group, but not the nonoliguric AKI group, was more likely to die (61% vs. 9%) and have neurodevelopmental impairment (41% vs. 14%) compare with the non-AKI group. After adjustment, oliguric (adjusted odds ratio [aOR], 8.97; 95% CI, 2.19-36.76), but not nonoliguric, AKI was associated with neurodevelopmental impairment. Neonatal oliguric AKI is associated with neurodevelopmental impairment in very preterm-birth children. Long-term head-size and neurodevelopmental follow-up after neonatal AKI is warranted.

Vibrio vulnificus pneumonia with multiorgan failure: a case report and review of the literature

BackgroundVibrio vulnificus is a gram-negative bacterium causing three clinical syndromes namely, gastrointestinal symptoms, skin sepsis and primary sepsis. Primary sepsis exhibits mortality rates exceeding 50%, particularly in the immunocompromised. Vibrio vulnificus is transmitted via consumption of contaminated seafood and contaminated seawater skin exposure. We describe a rare case of an immunocompetent male presenting with an atypical Vibrio vulnificus infection, culminating in severe pneumonia requiring intensive care.Case presentationA 46 year old Indian male dockyard worker, a non-smoker and teetotaler, of Indian origin presented to the emergency treatment unit of a tertiary care hospital in Sri Lanka, with fever, productive cough with yellow sputum, pleuritic chest pain and tachypnea for five days. He had no gastrointestinal or skin manifestations. His respiratory rate was 38 breaths/min, pulse rate was 120 bpm, blood pressure was 107/75 mmHg and pulse oximetry was 85% on air. Chest X-ray revealed consolidation of the left lung. Empiric intravenous Piperacillin-tazobactam and Clarithromycin were commenced after obtaining blood and sputum cultures. Over the next 24 h, his oxygen requirement rose and as he required vasopressor support, he was admitted to the intensive care unit. He was intubated and bronchoscopy was performed on day two, which demonstrated thick secretions from left upper bronchial segments. His antibiotics were changed to intravenous ceftriaxone and doxycycline following a positive blood culture report of Vibrio vulnificus. He was ventilated for ten days and his intensive care stay was complicated with a non-oliguric acute kidney injury, with serum creatinine rising up to 8.67 mg/dL (0.81–0.44 mg/dL). He developed mild thrombocytopenia with platelets dropping to 115 × 103 /uL (150–450 × 103/uL) which resolved spontaneously. Vasopressors were weaned off by day eight and the patient was extubated on day ten. He was discharged from intensive care on day twelve and made a full recovery.ConclusionsPneumonia itself is an atypical manifestation of Vibrio vulnificus and furthermore, this patient was immunocompetent and did not exhibit the classical gastro-intestinal and skin manifestations. This case highlights the occurrence of atypical Vibrio sp. infections in patients with high exposure risks and the need for early supportive and appropriate antibiotic therapies.

Preceding risks and mortality outcomes of different neonatal acute kidney injury in preterm infants.

The aim of the study was to examine preceding risks and mortality outcomes of oliguric and non-oliguric acute kidney injury (AKI) in very preterm infants. Infants born ≤30 weeks' gestation were included. AKI was diagnosed based on neonatal Kidney Disease: Improving Global Outcomes criteria and was classified as oliguric and non-oliguric according to the urine-output criteria. We used modified Poisson and Cox proportional-hazards models for statistical comparisons. Of 865 enrolled infants (gestational age 27.2 ± 2.2 weeks and birth weight 983 ± 288 gm), 204 (23.6%) developed AKI. Before AKI, the oliguric AKI group had significantly higher prevalence of small-for-gestational age (p = 0.008), lower 5-min Apgar score (p = 0.009) and acidosis (p = 0.009) on admission, and hypotension (p = 0.008) and sepsis (p = 0.001) during admission than the non-oliguric AKI group. Oliguric (adjusted risk ratio 3.58, 95% CI 2.33-5.51; adjusted hazard ratio 4.93, 95% CI 3.14-7.72) instead of non-oliguric AKI had significantly higher mortality risks than no AKI. Oliguric AKI showed significantly higher mortality risks than non-oliguric AKI, irrespective of serum creatinine and severity of AKI. Categorizing AKI as oliguric and non-oliguric was crucial because of the distinct preceding risks and mortality outcomes of these two types of AKI in very preterm neonates. The differences of the underlying risks and prognosis between oliguric and non-oliguric AKI in very preterm infants remain unclear. We found that oliguric AKI, but not non-oliguric AKI, carries higher mortality risks than infants without AKI. Oliguric AKI possessed higher mortality risks than non-oliguric AKI, irrespective of concomitant serum creatinine elevation and severe AKI. Oliguric AKI is more associated with prenatal small-for-the-gestational age and perinatal and postnatal adverse events, while non-oliguric AKI is associated with nephrotoxins exposures. Our finding highlighted the importance of oliguric AKI and is helpful in developing future protocol in neonatal critical care.

Abstract #1406558: Severe Renal Compromise Associated with Hypercalcemic Crisis Due to Giant Parathyroid Adenoma in a Woman with Bilateral Adrenal Incidentalomas

Parathyroid or hypercalcaemic crisis is a rare presenting manifestation of primary hyperparathyroidism (PHPT). We present a woman with severe hypercalcaemia due to giant parathyroid adenoma presenting as exacerbated chronic kidney disease, who was also found to have non-functioning bilateral adrenal adenomas. A 74-year-old woman, a history of arterial hypertension 10 years ago and lumbar spine scoliosis, usual medication irbersartan 150 mg/day, was admitted by emergency with a 1-week illness time characterized by lower limb weakness, severe low back pain, nausea and vomiting, which intensified the day of admission. Examination revealed BP 120/60 mmHg, heart rate 89 beats/min, weight 75kg, height 1.72cm, dry oral mucosa, no lymphadenopathy or nodules palpable at neck level. Laboratory tests: Arterial gases pH: 7.3, HCO3: 17mmol/L, Calcium: 3.8meq/L; hemoglobin: 10.1g/dl, creatinine: 7.32mg/dl, urea: 181mg/dl, sodium: 140mmol/L, potassium: 5mmol/L, calcium: 14.1mg/dl, phosphorus: 5.6mg/dl, magnesium: 2.18mg/dl. Renal ultrasound showed: signs of bilateral chronic kidney disease. Given the suspicion of malignancy and awaiting the result of parathormone (PTH), the body CT in the emergency room showed a solid lesion at the neck level, located posteriorly and in contact with the left thyroid lobe, measuring 39 x 14 x 30 mm, contacted the trachea and partially displaced the esophagus to the right without infiltrating them, it maintained interface with the left carotid and jugular, suggesting parathyroid dependence; and incidentally, both adrenal glands were diffusely thickened, the left showed a nodular formation of 20 x 15 mm, with an attenuation of -10 HU. She was hospitalized, received hydration, furosemide and pamidronate, did not require renal replacement therapy. Intact PTH was 1114 pg/mL; it was possible to normalize the levels of calcium, phosphorus, magnesium, creatinine decreased to 2.53mg/dl. Sestamibi scintigraphy showed an image compatible with lower left parathyroid adenoma and bone densitometry showed osteoporosis with a high risk of fracture (left forearm (1/3): bdm= 0.475g/cm2, Tscore= -5.3, hip: bdm= 0.435g /cm2, tscore= -4.5). The patient underwent a lower left parathyroidectomy, where a 5x3.5cm parathyroid tumor was reported with an increased consistency of brown coloration; the pathology reported giant adenoma of the parathyroid gland with apoplexy. In the postoperative period, the intact PTH was 57 pg/ml, at the same time the functionality of the adrenal adenoma was ruled out. She developed hungry bone syndrome for which she receives calcium and calcitriol to this day. Some studies provided an unclear definition of hypercalcemic crisis as a serum calcium concentration >3.5 mmol/L, accompanied by signs and symptoms. A hypercalcemic crisis was first described in 1939 by Hanes, and is considered as an endocrine emergency and fatal in the absence of optimal treatment. The acute effects of PHPT on renal function are not well understood. Furthermore, non-oliguric acute kidney injury caused by refractory hypercalcemia requires emergent hemodialysis, which was not necessary in our patient.

Synthetic cannabinoid-associated acute interstitial nephritis: An emerging cause of pediatric acute kidney injury?

Synthetic cannabinoid (SCB) usage among children is a rapidly emerging public health concern in the United States. Acute kidney injury (AKI) is an uncommon manifestation of SCB usage, with acute tubular necrosis (ATN) as the predominant histology. Here we describe a 16-year-old adolescent who sustained severe non-oliguric AKI in association with SCB usage. Emesis, right flank pain, and hypertension were the presenting clinical features. There was no uveitis, skin rash, joint pains, or eosinophilia. Urinalysis showed absence of proteinuria or hematuria. Urine toxicology was negative. Renal sonogram showed bilateral echogenic kidneys. Renal biopsy demonstrated severe acute interstitial nephritis (AIN), mild tubulitis, and absence of ATN. AIN responded with pulse steroid followed by oral steroid. Renal replacement therapy was not required. Although the exact pathophysiology of SCB-associated AIN is not known, immune response elicited by the renal tubulointerstitial cells against the antigens present in the SCB is the most likely mechanism. A high index of suspicion for SCB-induced AKI is necessary in adolescents who present with AKI of unclear etiology.

47-Year-Old Woman With Bilateral Flank Pain

47-Year-Old Woman With Bilateral Flank Pain

Acute Kidney Injury in a Case of Multiorgan Failure, Disseminated Intravascular Coagulation and Purpura Fulminans

Introduction Purpura fulminans (PF) is a life-threatening syndrome consisting of Disseminated Intravascular Coagulation (DIC), thrombotic occlusion of small- and medium-sized blood vessels with skin necrosis. Although there are few studies in the literature, only a minority of them discuss renal manifestations. Case Report We present a case of a 57-year-old Caucasian female with acute kidney injury (AKI) in the setting of multiorgan failure (MOF), DIC and PF. She presented with fever, exudative drainage from her port site, and skin changes concerning for bacteremia. Empiric antibiotics were started after blood, urine, and wound cultures were obtained. None of the cultures grew any organisms. Fever resolved after port removal. She exhibited thrombocytopenia, leukopenia, and neutropenia. Urinalysis showed hyaline casts and a fractional excretion of urea (FeUrea) ≤35% indicating a pre-renal state. Her hospital course was complicated by atrial fibrillation, acute hypoxic respiratory failure requiring mechanical ventilation, and hypovolemic shock requiring pressor support. Further, complicated by multiorgan failure including non-oliguric AKI and heart failure with reduced ejection fraction (HFrEF) of ≤65%. Acute skin findings included dusky, purple macules and patches involving all digits of both hands as well as gangrenous changes on the face and toes. It prompted further investigation by Hematology and Dermatology. Skin biopsy showed early leukocytoclastic vasculitis changes. Her laboratory markers were suggestive of DIC and Purpura Fulminans.

Clinical courses and features of renal tubular damage in 5 patients with anorexia nervosa and non-oliguric acute kidney injury

Clinical courses and features of renal tubular damage in 5 patients with anorexia nervosa and non-oliguric acute kidney injury

Acquired Bartters Syndrome: A Rare Metabolic Abnormality Induced by Streptomycin

Streptomycin associated nephrotoxicity can manifest either as nonoliguric acute kidney injury, tubular dysfunction or electrolyte abnormalities including Fanconi-like syndrome or Bartter syndrome. We report a case of Streptomycin-induced renal electrolyte wasting mimicking Bartter’s syndrome.

Changes in hemodynamics, renal blood flow and urine output during continuous renal replacement therapies

Continuous renal replacement therapies (CRRT) affect hemodynamics and urine output. Some theories suggest a reduced renal blood flow as the cause of the decreased urine output, but the exact mechanisms remain unclear. A prospective experimental study was carried out in 32 piglets (2–3 months old) in order to compare the impact of CRRT on hemodynamics, renal perfusion, urine output and renal function in healthy animals and in those with non-oliguric acute kidney injury (AKI). CRRT was started according to our clinical protocol, with an initial blood flow of 20 ml/min, with 10 ml/min increases every minute until a goal flow of 5 ml/kg/min. Heart rate, blood pressure, central venous pressure, cardiac output, renal blood flow and urine output were registered at baseline and during the first 6 h of CRRT. Blood and urine samples were drawn at baseline and after 2 and 6 h of therapy. Blood pressure, cardiac index and urine output significantly decreased after starting CRRT in all piglets. Renal blood flow, however, steadily increased throughout the study. Cisplatin piglets had lower cardiac index, higher vascular resistance, lower renal blood flow and lower urine output than control piglets. Plasma levels of ADH and urine levels of aquaporin-2 were lower, whereas kidney injury biomarkers were higher in the cisplatin group of piglets. According to our findings, a reduced renal blood flow doesn’t seem to be the cause of the decrease in urine output after starting CRRT.

Valacyclovir Non-Oliguric Acute Kidney Injury: a Case Report of 84 Year-Old Female

Valacyclovir Non-Oliguric Acute Kidney Injury: a Case Report of 84 Year-Old Female

Positron emission tomography as an adjuvant diagnostic test in the evaluation of checkpoint inhibitor-associated acute interstitial nephritis

BackgroundAcute interstitial nephritis is an immune-related adverse event that can occur in patients receiving immune checkpoint inhibitor therapy. Differentiating checkpoint inhibitor-associated acute interstitial nephritis from other causes of acute kidney injury in patients with cancer is challenging and can lead to diagnostic delays and/or unwarranted immunosuppression. In this case report, we assess the use of 18F-flourodeoxyglucose positron-emission tomography imaging as an alternative diagnostic modality in the evaluation of potential acute interstitial nephritis.Case presentationA 55-year-old woman with metastatic vulvar melanoma underwent treatment with two cycles of ipilimumab plus nivolumab, followed by seven cycles of nivolumab combined with radiation therapy. During her treatment, she developed non-oliguric acute kidney injury to a creatinine of 4.5 mg/dL from a baseline of 0.5 mg/dL. A clinical diagnosis of acute interstitial nephritis was made, and steroids were initiated, with rapid improvement of her acute kidney injury. Retrospectively, four positron-emission tomography scans obtained for cancer staging purposes were reviewed. We found a markedly increased 18F-flourodeoxyglucose uptake in the renal cortex at the time acute interstitial nephritis was diagnosed compared to baseline. In three cases of acute kidney injury due to alternative causes there was no increase in 18F-flourodeoxyglucose uptake from baseline.ConclusionsTo our knowledge, this is the first report describing increased 18F-flourodeoxyglucose uptake in the renal cortex in a patient with checkpoint inhibitor-associated acute interstitial nephritis. Our findings suggest that 18F-flourodeoxyglucose positron-emission tomography may be a valuable test for diagnosing immune-mediated nephritis, particularly in patients where timely kidney biopsy is not feasible.

Correction: Cisplatin-Induced Non-Oliguric Acute Kidney Injury in a Pediatric Experimental Animal Model in Piglets.

[This corrects the article DOI: 10.1371/journal.pone.0149013.].